‹ Pathophysiology Hub Exam 1 Study Guide
PATHOPHYSIOLOGY

Exam 1 Master Study Guide

Modules 1 & 2: Fluids, Electrolytes, ABGs, Pathogens & Immune Disorders
ⓘ What's on Exam 1

Fifty questions, mixing multiple choice with select-all-that-apply. Every topic below is fair game.

Use this guide as the road map. Then practice with the answers hidden.

ⓘ How to use this guide
  • Click any topic card to jump to it. Click the title bar to open or close it.
  • Answers are hidden. Try first. Then click "Show answer." Pulling the answer out of your own head is what builds memory.
  • Each topic has: content, a memory aid, a common mix-up, free-response questions, multiple-choice questions, a clinical case, and a checklist.
  • To save a PDF: press Ctrl+P in your browser (Cmd+P on a Mac). Then pick "Save as PDF." Every closed section opens by itself for printing.
📅 14-Day Study Schedule, Built for Exam Week ▼
DayFocus
Day 1–2Topics 1–2 (fluid compartments, hormones). Learn ICF vs ECF by heart.
Day 3–4Topic 3 (electrolytes). Learn the lab values for Na, K, Ca, P, Mg.
Day 5–6Topics 4–5 (acid-base, buffer systems, acidosis/alkalosis).
Day 7Topic 6 (reading ABGs). Work through ALL 4 examples.
Day 8–9Topics 7–9 (pathogens, stages of infection, UTIs).
Day 10–11Topics 10–11 (immunity, immunoglobulins, hypersensitivity, transplants).
Day 12Topic 12 (HIV/AIDS, weak immune systems, autoimmune disease, leukemia/lymphoma).
Day 13Redo every answer you missed. Run through the cheat sheet.
Day 14Light review only. Sleep. Eat. Drink water. Take the exam.

📋 Topic Navigator

TOPIC 1 · WEEK 1
Fluid Compartments & Pressures
TOPIC 2 · WEEK 1
Fluid Regulation Hormones
TOPIC 3 · WEEK 1
Electrolyte Imbalances
TOPIC 4 · WEEK 1
Acid-Base & Buffers
TOPIC 5 · WEEK 1
Acidosis & Alkalosis Causes
TOPIC 6 · WEEK 1
ABG Interpretation
TOPIC 7 · WEEK 2
Pathogens & Resistance
TOPIC 8 · WEEK 2
Infection Stages & TB
TOPIC 9 · WEEK 2
UTIs: Cystitis vs Pyelo
TOPIC 10 · WEEK 2
Immunity & Immunoglobulins
TOPIC 11 · WEEK 2
Hypersensitivity & Transplant
TOPIC 12 · WEEK 2
HIV, Immunodeficiency, Cancers
🎯 Rapid-Review Cheat Sheet 🧪 Lab Values 📚 Glossary

🧪 Normal Lab Values You MUST Know

ValueNormal RangeMemory Hint
Sodium (Na⁺)135–145 mEq/LWidest range. Drives fluid balance
Potassium (K⁺)3.5–5.0 mEq/LHeart rhythm. Narrow range
Calcium (Ca)8.5–10.5 mg/dLMuscles, nerves, clotting
Phosphate (P)2.5–4.5 mg/dLMoves OPPOSITE calcium
Magnesium (Mg)1.5–2.5 mEq/LRelaxes muscle. Blocks calcium at the nerve ending
pH7.35–7.45<7.35 = acidosis. >7.45 = alkalosis
PaCO₂35–45 mmHgAcid from the lungs (high = more acid)
HCO₃⁻22–26 mEq/LBase from the kidneys (high = more base)
PaO₂80–100 mmHgHow well blood is carrying oxygen
TOPIC 1 💦 Fluid Compartments & Pressures MUST KNOW▼

Where Body Water Lives

Compartment% of Body FluidDominant Electrolyte
Intracellular (ICF)~2/3 (~67%)High Potassium (K⁺)
Extracellular (ECF)~1/3 (~33%)High Sodium (Na⁺)

The ECF splits into three parts:

  • Intravascular fluid, the fluid inside blood vessels (plasma).
  • Interstitial fluid, the fluid in the spaces around cells.
  • Transcellular fluid, smaller pools like spinal fluid, joint fluid, and belly fluid.

Hydrostatic vs. Oncotic Pressure

👉 HYDROSTATIC pressure
A "pushing" force from the blood inside the vessel. It pushes fluid OUT of capillaries into tissue.

What raises it? High BP, heart failure, too much IV fluid, blocked blood return.
👈 ONCOTIC pressure
A "pulling" force. It comes mostly from albumin, a protein in plasma. It pulls fluid INTO the vessel.

What lowers it? Liver failure (makes less albumin), poor diet (no protein coming in), kidney disease (albumin leaks into urine).

Causes of Peripheral Edema (fluid in the tissues)

Edema means fluid leaks out of vessels into tissue. It happens when:

  • Hydrostatic pressure goes UP → fluid gets pushed out too hard (heart failure, high blood pressure).
  • Oncotic pressure goes DOWN → nothing pulls the fluid back in (liver failure, poor diet, kidney disease that loses albumin).
  • Lymph vessels are blocked → fluid cannot drain away (lymphedema, after breast surgery).
  • Capillaries turn leaky → the vessel walls let fluid through (inflammation, sepsis, burns).
💡 Memory aid: Hydrostatic = "Hose pushing out." Oncotic = "Owe me back," since albumin pulls. Edema means the pushers beat the pullers.
⚠️ Common mix-up: Sodium is the main electrolyte outside the cell (ECF). Potassium is the main one inside (ICF). Many people swap these two.

❓ Free-Response Practice

  1. What percent of body fluid is inside cells vs outside cells? Which electrolyte leads in each?
    Show answer
    ICF is about 2/3 and is high in K⁺. ECF is about 1/3 and is high in Na⁺.
  2. Compare hydrostatic and oncotic pressure.
    Show answer
    Hydrostatic is a pushing force. It pushes fluid OUT of vessels. Oncotic is a pulling force from albumin. It pulls fluid INTO vessels.
  3. List 4 causes of edema in the legs and arms.
    Show answer
    Higher hydrostatic pressure (heart failure). Lower oncotic pressure from low albumin (liver failure, poor diet, kidney disease). Blocked lymph vessels. Leaky capillaries (inflammation or sepsis).
  4. What is the difference between intravascular and interstitial fluid?
    Show answer
    Intravascular fluid sits inside blood vessels (plasma). Interstitial fluid sits around tissue cells, outside the vessels.
  5. Why does a patient with cirrhosis get edema and ascites?
    Show answer
    The scarred liver makes less albumin. That drops oncotic pressure. Fluid then stays in the tissues and belly instead of being pulled back into the vessels.

✅ Multiple Choice Practice

  1. The main electrolyte inside cells is:
    A) Sodium · B) Potassium · C) Calcium · D) Chloride
    Show answer
    B. Potassium dominates ICF.
  2. A patient with bad burns swells all over. The most likely cause is:
    A) Blocked lymph vessels · B) Leaky capillaries · C) Low hydrostatic pressure · D) High oncotic pressure
    Show answer
    B. A burn makes capillaries leaky. Fluid escapes into the tissue.
  3. Which protein does most of the work of oncotic pressure?
    A) Hemoglobin · B) Globulin · C) Albumin · D) Fibrinogen
    Show answer
    C. Albumin.
🩺 Clinical Scenario
A 68-year-old with congestive heart failure has 3+ pitting edema in both ankles and trouble breathing. Albumin is normal. Explain how the edema formed. Explain why the lung symptoms showed up.
Show answer
Heart failure makes blood back up in the veins. That raises hydrostatic pressure in the capillaries. Fluid gets pushed out into the tissue, so the ankles swell. When the backup is on the left side of the heart, pressure rises in the lung capillaries. Fluid then leaks into the air sacs. That is pulmonary edema, and it causes shortness of breath and crackles. Albumin is normal because the problem is hydrostatic, not oncotic.
☑ Self-Assessment Checklist
  • I can give the ICF and ECF percentages and the main electrolyte in each.
  • I can split the ECF into intravascular, interstitial, and transcellular.
  • I can describe hydrostatic and oncotic pressure and say what each one does.
  • I can list at least 4 causes of edema in the legs and arms.
  • I can explain what albumin does for fluid balance.
↑ Back to top
TOPIC 2 🧡 Fluid Regulation Hormones: RAAS, ADH, ANP/BNP MUST KNOW▼

The RAAS System (Renin-Angiotensin-Aldosterone System)

What turns it on: the kidneys sense low blood pressure, low blood volume, or low sodium.

The chain of steps:

  1. The kidneys release renin when BP or volume is low.
  2. Renin turns angiotensinogen from the liver into angiotensin I.
  3. ACE (angiotensin-converting enzyme) in the lungs turns angiotensin I into angiotensin II.
  4. Angiotensin II then does 2 main jobs:
    • It tightens blood vessels → BP goes up.
    • It tells the adrenal cortex to release aldosterone.

Aldosterone vs. ADH: What Each Does at the Kidney

HormoneFromKidney EffectNet Effect
AldosteroneAdrenal cortexTakes back Na⁺, and water with it. Dumps K⁺↑ BP, ↑ volume, ↓ K⁺
ADH (Vasopressin)Posterior pituitaryTakes back water only, no sodium↑ BP, ↑ volume, makes urine stronger

ANP & BNP, The "Off-Switch"

ANP (atrial natriuretic peptide) comes from the atria of the heart. BNP (brain or B-type natriuretic peptide) comes from the ventricles. Both come out when the heart gets stretched by high volume or high pressure.

What they do: the opposite of RAAS.

  • Dump sodium in the urine (natriuresis) and water with it.
  • Widen blood vessels.
  • Lower BP and volume.
  • Block renin and aldosterone.

Why it matters: a high BNP is a sign of heart failure.

Angiotensin II: Main Actions

  • Tightens vessels → BP goes up.
  • Tells the body to release aldosterone.
  • Tells the body to release ADH.
  • Makes you thirsty.

This is why ACE inhibitors lower BP. These are the "–pril" drugs like lisinopril. They block this whole chain.

💡 Memory aids:
  • RAAS = "Raises pressure." Low BP turns RAAS on. It saves Na and water. BP goes up.
  • ANP/BNP = "Anti-pressure." High pressure stretches the heart. ANP and BNP come out. They dump Na and water. BP goes down.
  • Aldosterone = "Aldo loves sodium."
  • ADH = "Anti-Diuretic," so it holds on to water.
⚠️ Common mix-up: Aldosterone keeps sodium and water. ADH keeps ONLY water, no sodium. So in SIADH, where there is too much ADH, the blood sodium drops. The water dilutes it, which is why it is called dilutional hyponatremia.

❓ Free-Response Practice

  1. What turns the RAAS system on?
    Show answer
    The kidneys sense low BP, low blood volume, or low sodium.
  2. List the 4 main actions of angiotensin II.
    Show answer
    It tightens vessels. It triggers aldosterone. It triggers ADH. It makes you thirsty.
  3. Compare what aldosterone and ADH do at the kidney.
    Show answer
    Aldosterone takes back sodium, and water follows it. It also dumps potassium. ADH takes back water only, with no sodium.
  4. What do ANP and BNP do?
    Show answer
    They dump sodium and water. They widen vessels. They lower BP and volume. They block RAAS. They are the mirror image of RAAS.
  5. Why is BNP high in heart failure?
    Show answer
    Backed-up fluid overstretches the failing ventricles. That stretch makes them release BNP. More BNP means more stretch, and more stretch means worse failure.

✅ Multiple Choice Practice

  1. Aldosterone makes the kidneys:
    A) Dump sodium · B) Take back sodium and water, and dump potassium · C) Take back water only · D) Widen vessels
    Show answer
    B. It takes back Na, and water with it. It dumps K.
  2. A high BNP points most directly to:
    A) Liver failure · B) Dehydration · C) Heart failure · D) Diabetes
    Show answer
    C. Heart failure, from stretched ventricles.
  3. Which hormone takes back water WITHOUT moving sodium?
    A) Aldosterone · B) ADH · C) Angiotensin II · D) Renin
    Show answer
    B. ADH moves water only.
🩺 Clinical Scenario
A trauma patient has lost a lot of blood. Which RAAS steps does the body use to compensate? What would you expect in the vital signs and urine output before treatment?
Show answer
Low volume makes the kidneys release renin. Renin leads to angiotensin II. Angiotensin II tightens vessels, so BP comes up a little and the heart rate rises. It also brings out aldosterone and ADH, so the kidneys hold on to sodium and water. Expect a fast heart rate, a narrow pulse pressure, less urine (oliguria), and dark, concentrated urine. Giving IV fluid shuts the whole chain back down.
☑ Self-Assessment Checklist
  • I can list what turns RAAS on and follow renin through to angiotensin II.
  • I can name the 4 main actions of angiotensin II.
  • I can compare aldosterone (Na, water, and K loss) with ADH (water only).
  • I can describe how ANP and BNP work against RAAS.
  • I can explain why BNP is used as a heart failure marker.
↑ Back to top
TOPIC 3 🧪 Electrolyte Imbalances (Na, K, Ca, P, Mg) MUST KNOW▼

Hint: Water follows sodium. Potassium is "the heart one." Phosphate moves opposite to calcium. Magnesium blocks calcium at the nerve ending.

⚒ Sodium (Na⁺): 135–145 mEq/L

What it does: runs fluid balance. The kidneys control it.

Hyponatremia (<135)Hypernatremia (>145)
CausesSIADH, diuretics, vomiting or diarrhea, too much water, heart failure (the blood gets watered down)Dehydration, diabetes insipidus, too much salt intake, burns
S/SxHeadache, confusion, sleepiness, seizures, muscle cramps. The brain swells, because the cells pull in water.Thirst, dry mouth, crankiness, sleepiness, seizures. The cells shrink.

❤️ Potassium (K⁺): 3.5–5.0 mEq/L, "the heart one"

What it does: sets the resting voltage across the cell membrane, so it runs how easily nerve and heart cells fire and how the beat is carried. It also helps with acid-base balance. The squeeze itself belongs to calcium.

Hypokalemia (<3.5)Hyperkalemia (>5.0)
CausesDiuretics (loop ones most of all), vomiting or diarrhea, alkalosis, low intake, suction through an NG tubeKidney failure, acidosis, K-sparing diuretics, damaged tissue (burns or crush injury), Addison's disease
S/SxWeak muscles, tiredness, leg cramps, constipation, flat T waves and U waves on the EKG, odd heart rhythmsWeak muscles, tingling, peaked T waves on the EKG, odd heart rhythms, cardiac arrest

🧹 Calcium (Ca): 8.5–10.5 mg/dL

What it does: helps muscles squeeze, lets nerves fire, helps blood clot, and keeps bone strong.

Hypocalcemia (<8.5)Hypercalcemia (>10.5)
CausesLow parathyroid hormone, too little vitamin D, kidney disease, poor gut absorption, pancreatitisToo much parathyroid hormone, cancer that has spread to bone, too much vitamin D, long bed rest
S/SxTwitching muscles, tetany (locked-up spasms), Trousseau's sign (hand spasm), Chvostek's sign (face twitch), tingling, seizuresWeak muscles, bone pain, kidney stones, constipation, sleepiness. "Bones, stones, groans, psychic moans."

🧸 Phosphate (P): 2.5–4.5 mg/dL, the opposite of calcium

What it does: steadies cell membranes, builds bone and teeth, powers cells, and builds DNA and RNA.

Hypophosphatemia (<2.5)Hyperphosphatemia (>4.5)
CausesAlcohol use disorder, burns, refeeding syndrome, poor gut absorptionKidney failure, which is the most common cause
S/SxSore, weak muscles, crankiness, constipation, confusionMuscle cramps, bone pain, itching (pruritus). The signs copy low calcium, since Ca falls as P climbs

🧋 Magnesium (Mg): 1.5–2.5 mEq/L, "the muscle relaxer"

What it does: relaxes muscle and helps control potassium. It blocks calcium at the nerve ending, so it damps down how much signal the nerve sends to the muscle.

Hypomagnesemia (<1.5)Hypermagnesemia (>2.5)
CausesAlcohol use disorder, poor gut absorption, diarrhea, diureticsKidney failure, antacids or laxatives that contain Mg, IV Mg given for preeclampsia
S/SxLooks just like low calcium. Tetany, twitching, Trousseau's and Chvostek's signs, odd heart rhythms, seizuresSleepiness, low blood pressure, weak deep tendon reflexes, slow breathing, cardiac arrest
💡 Master pattern:
  • Calcium ↔ Phosphate: when one goes up, the other goes down.
  • Calcium ↔ Magnesium: magnesium blocks calcium at the nerve ending, but the two lab values often move together. Both run low in alcohol use disorder. In kidney failure magnesium climbs while calcium falls, so do not pair them there.
  • Low calcium and low magnesium look the same: tetany, Trousseau's, Chvostek's.
  • EKG changes: high K gives peaked T waves. Low K gives flat T waves and U waves.
⚠️ Common mix-up: "Hypo" and "hyper" can cause the SAME symptom. Muscle weakness shows up in both high and low potassium. So look at the lab value and the specific signs, like peaked vs flat T waves, to tell them apart.

❓ Free-Response Practice

  1. Give the normal lab range for Na, K, Ca, P, and Mg.
    Show answer
    Na: 135–145 mEq/L. K: 3.5–5.0 mEq/L. Ca: 8.5–10.5 mg/dL. P: 2.5–4.5 mg/dL. Mg: 1.5–2.5 mEq/L.
  2. Which EKG change goes with high potassium? Which goes with low potassium?
    Show answer
    High potassium gives peaked T waves. Low potassium gives flat T waves with tall U waves.
  3. Describe Trousseau's and Chvostek's signs. Which imbalance do they point to?
    Show answer
    Trousseau's sign is a hand spasm after you inflate a BP cuff. Chvostek's sign is a face twitch when you tap the cheek. Both point to low calcium, and low magnesium can do it too.
  4. Why does kidney failure raise phosphate AND drop calcium?
    Show answer
    Failing kidneys cannot clear phosphate, so P builds up. Calcium and phosphate move in opposite directions, so Ca drops as P rises. Failing kidneys also turn on less vitamin D. That means the gut absorbs even less calcium.
  5. What are the signs of too much magnesium (hypermagnesemia)?
    Show answer
    Weak deep tendon reflexes, sleepiness, low blood pressure, slow breathing, cardiac arrest. This is why reflexes are checked during IV Mg for preeclampsia.

✅ Multiple Choice Practice (SATA practice too)

  1. Which lab finding fits high potassium best?
    A) Flat T waves · B) Peaked T waves · C) Long QT · D) U waves
    Show answer
    B. Peaked T waves.
  2. Select ALL that apply. Causes of low potassium:
    A) Loop diuretics · B) Vomiting · C) Kidney failure · D) Alkalosis · E) Acidosis
    Show answer
    A, B, D. Loop diuretics waste K. Vomiting loses K. Alkalosis pushes K into cells, so blood K reads low. Kidney failure and acidosis raise K instead.
  3. A patient with low calcium is likely to show:
    A) Bone pain · B) Constipation · C) Trousseau's sign · D) Sleepiness
    Show answer
    C. Trousseau's sign, a hand spasm when the BP cuff inflates.
🩺 Clinical Scenario
A patient with chronic kidney disease has these labs: K⁺ 6.1, Ca 7.8, P 6.5. The patient feels weak and has tingling around the mouth. Which two abnormal labs are tied together? What would the EKG most likely show?
Show answer
The Ca of 7.8 is low and the P of 6.5 is high. These two are tied together. Failing kidneys cannot clear P, and Ca moves opposite to P. The tingling comes from the low calcium. The K of 6.1 is high because the kidneys cannot clear K either. The EKG would show peaked T waves. Treatment may include calcium gluconate to steady the heart. It also includes steps to drop the K, such as insulin with D50, kayexalate, or dialysis.
☑ Self-Assessment Checklist
  • I can say the normal ranges for Na, K, Ca, P, and Mg from memory.
  • I can list at least 3 causes and 3 signs for each high and low electrolyte.
  • I can name the EKG findings for low and high potassium.
  • I can describe Trousseau's and Chvostek's signs.
  • I can explain why kidney failure ties high P, low Ca, and high K together.
↑ Back to top
TOPIC 4 ⚖ Acid-Base Foundations & Buffer Systems MUST KNOW▼

Acid-Base Basics

  • Normal body chemistry makes CO₂ and H⁺. Both of these are acids.
  • The body's goal is to hold pH between 7.35 and 7.45. That is a very narrow window.
  • pH and H⁺ move in opposite directions. When H⁺ is high, pH is low, and the blood is acidic.
  • Acids: CO₂ and H⁺. Base: HCO₃⁻.

The 3 Buffer Systems

BufferSpeedHow It Works
Serum (chemical)Right away, in secondsProteins grab H⁺. K⁺ trades places with H⁺ across the cell membrane
RespiratoryMinutesThe lungs change how fast you breathe. Breathing faster blows off CO₂, so pH rises. Breathing slower holds CO₂ in, so pH falls. Kussmaul breathing is deep and fast, and you see it in DKA
Renal2–3 days, and it is the STRONGESTThe kidneys dump H⁺ and take back or make HCO₃⁻

Why K⁺ Shifts When pH Shifts

In acidosis, H⁺ pours into the cells to be buffered. K⁺ gets pushed out into the blood. So acidosis goes with high potassium. Alkalosis does the reverse, so alkalosis goes with low potassium.

💡 Memory aids:
  • CO₂ = ACID. High CO₂ means acidic.
  • HCO₃⁻ = BASE. High HCO₃⁻ means alkaline.
  • "Acidosis = K up." "Alkalosis = K down."
⚠️ Common mix-up: A lower pH means MORE acid, not less. The smaller number means more H⁺.

❓ Free-Response Practice

  1. Give all 4 normal ABG values.
    Show answer
    pH 7.35–7.45 · PaCO₂ 35–45 mmHg · HCO₃⁻ 22–26 mEq/L · PaO₂ 80–100 mmHg.
  2. Which one is the acid and which one is the base: CO₂ or HCO₃⁻?
    Show answer
    CO₂ is the acid. HCO₃⁻ is the base.
  3. Put the 3 buffer systems in order of speed.
    Show answer
    Serum works in seconds. The lungs work in minutes. The kidneys take days, and they are the strongest.
  4. What is Kussmaul breathing?
    Show answer
    Deep, fast breathing. It blows off CO₂ to make up for metabolic acidosis. You see it most often in DKA.
  5. What does acidosis do to blood K⁺?
    Show answer
    It raises it. H⁺ moves into the cells, and K⁺ gets pushed out into the blood.

✅ Multiple Choice Practice

  1. Which buffer acts fastest?
    A) Serum · B) Respiratory · C) Renal · D) Lymphatic
    Show answer
    A. The serum (chemical) buffer works in seconds.
  2. The strongest buffer system is:
    A) Serum · B) Respiratory · C) Renal · D) Cardiac
    Show answer
    C. The kidneys are the slowest but the strongest.
  3. A pH of 7.30 with a PaCO₂ of 50 mmHg means:
    A) Metabolic acidosis · B) Respiratory acidosis · C) Metabolic alkalosis · D) Respiratory alkalosis
    Show answer
    B. An acid pH with a high CO₂ is respiratory acidosis.
🩺 Clinical Scenario
A patient in DKA is breathing fast and deep. Which buffer system is at work, and why?
Show answer
DKA makes metabolic acidosis, because ketones are acids. The respiratory buffer kicks in. The patient breathes hard to blow off CO₂, which is an acid, so the pH comes up. That deep, fast breathing is called Kussmaul respirations.
☑ Self-Assessment Checklist
  • I know all 4 normal ABG values by memory.
  • I can name CO₂ as the acid and HCO₃⁻ as the base.
  • I can rank the 3 buffer systems by speed and say which is strongest.
  • I can predict which way K⁺ moves in acidosis and in alkalosis.
↑ Back to top
TOPIC 5 🧪 Acidosis & Alkalosis Causes MUST KNOW▼

Acidosis (pH < 7.35)

TypeCausesWhat You See
Metabolic acidosisAcid added, so the gap goes wide: DKA (ketones) · lactic acidosis · salicylates · kidney failure. Bicarbonate lost, so the gap stays normal: bad diarrhea · renal tubular acidosisWide anion gap when acid is added, normal gap when HCO₃⁻ is lost · high potassium · Kussmaul breathing to compensate
Respiratory acidosisBreathing too little: COPD, pneumonia, opioid overdose, heavy sedationHypercapnia, which means ↑CO₂ · high potassium

Alkalosis (pH > 7.45)

TypeCausesWhat You See
Metabolic alkalosisHeavy vomiting · NG suction, which loses H⁺ · too much calcium carbonate from antacidsLow potassium
Respiratory alkalosisBreathing too much: panic, anxiety, fever, pain, a ventilator set too highHypocapnia, which means ↓CO₂ · low potassium

What Acidosis Does to the Body

  • Brain: confusion, sleepiness, coma.
  • Heart: odd rhythms, a weaker squeeze, wide vessels, low blood pressure.
  • Lungs: Kussmaul breathing, which is the body compensating.
  • Bone: long-term acidosis pulls Ca out of bone.
  • Electrolytes: potassium goes up.
  • Enzymes: they lose their shape at an extreme pH.
💡 Quick patterns:
  • Vomiting or NG suction = ALKALOSIS, because you lose stomach acid.
  • Diarrhea = ACIDOSIS, because you lose HCO₃⁻ from the gut.
  • DKA = METABOLIC ACIDOSIS.
  • COPD/opioid = RESPIRATORY ACIDOSIS.
  • Panic attack = RESPIRATORY ALKALOSIS.
⚠️ Common mix-up: Which end of the gut is losing fluid matters. The upper gut (vomiting) loses acid, so you get alkalosis. The lower gut (diarrhea) loses base, so you get acidosis.

❓ Free-Response Practice

  1. List 2 causes of metabolic acidosis and 2 causes of respiratory acidosis.
    Show answer
    Metabolic: DKA and bad diarrhea. Respiratory: COPD and opioid overdose.
  2. List 2 causes of metabolic alkalosis and 2 causes of respiratory alkalosis.
    Show answer
    Metabolic: heavy vomiting and NG suction. Respiratory: a panic attack and fast breathing from fever.
  3. Which way does K⁺ move in each acid-base problem?
    Show answer
    Acidosis pushes K⁺ up. Alkalosis pulls K⁺ down.
  4. List 3 things acidosis does to the body.
    Show answer
    Confusion or coma. Odd heart rhythms. High potassium. Kussmaul breathing to compensate. Over time, Ca loss from bone.
  5. What does a wide anion gap tell you?
    Show answer
    It means metabolic acidosis with extra acid built up that the lab did not measure. Think DKA, lactic acidosis, salicylates, or kidney failure.

✅ Multiple Choice Practice

  1. Heavy vomiting is most likely to cause:
    A) Metabolic acidosis · B) Metabolic alkalosis · C) Respiratory acidosis · D) Respiratory alkalosis
    Show answer
    B. You lose HCl from the stomach, so you get metabolic alkalosis.
  2. A patient with an opioid overdose is at highest risk for:
    A) Metabolic acidosis · B) Metabolic alkalosis · C) Respiratory acidosis · D) Respiratory alkalosis
    Show answer
    C. Slow breathing traps CO₂ in the blood.
  3. Bad diarrhea is most likely to cause:
    A) Metabolic acidosis · B) Metabolic alkalosis · C) Respiratory acidosis · D) Respiratory alkalosis
    Show answer
    A. You lose HCO₃⁻ from the gut, so you get metabolic acidosis.
🩺 Clinical Scenario
A patient with COPD comes in short of breath, and it is getting worse. The ABG reads pH 7.30, PaCO₂ 60 mmHg, HCO₃⁻ 30 mEq/L. Name the disorder. Say what is compensating. Predict the K⁺.
Show answer
The pH is acidic. The CO₂ is high while the pH went down, so Respiratory Opposite makes the lungs the cause. The HCO₃⁻ is high, which is the kidneys compensating. So this is respiratory acidosis with partial metabolic compensation. Expect high potassium. Treat the cause. Help the patient move more air, give bronchodilators, and use oxygen carefully.
☑ Self-Assessment Checklist
  • I can list 2 causes for each of the 4 acid-base disorders.
  • I can predict which way K⁺ moves in acidosis and alkalosis.
  • I can list 3 things acidosis does to the body.
  • I can match a patient's condition to its likely acid-base disorder.
↑ Back to top
TOPIC 6 🧬 ABG Interpretation, Step by Step with Worked Cases MUST KNOW▼

Why we draw ABGs

An ABG shows three things. It shows oxygen (PaO₂), air movement (PaCO₂), and acid-base balance. That makes it key in the ICU, on a ventilator, and in metabolic emergencies.

The 3-Step ABG Method

  1. Look at the pH: under 7.35 is acidosis. Over 7.45 is alkalosis. A pH of 7.35–7.45 is normal, though it may be compensated.
  2. Decide if it is respiratory or metabolic, using ROME:
    • Check the PaCO₂, which is the lung value. Normal is 35–45 mmHg.
    • Check the HCO₃⁻, which is the kidney value. Normal is 22–26 mEq/L.
    • Respiratory Opposite: if the CO₂ moved the opposite numeric way from the pH, meaning one went up while the other went down, the lungs are the cause.
    • Metabolic Equal: if the HCO₃⁻ moved the same numeric way as the pH, meaning both went down or both went up, the kidneys are the cause.
  3. Look for compensation: if the OTHER value is also off, and it is pulling the pH back toward normal rather than driving it further out, the body is compensating.

ROME Memory Trick

ROMEWhat It Stands For
RespiratoryOpposite. The pH and the CO₂ move in OPPOSITE directions
MetabolicEqual. The pH and the HCO₃⁻ move in the SAME direction

Compensation Levels

  • Uncompensated. Only the value causing the problem is off.
  • Partly compensated. Both values are off, and the pH is still out of range.
  • Fully compensated. Both values are off, but the pH is back in range.

Worked Examples

Case 1: pH 7.29 · CO₂ 52 mmHg · HCO₃⁻ 24 mEq/L

Step 1: The pH of 7.29 is acidic.

Step 2: The CO₂ of 52 is high while the pH went down, so the two moved in opposite numeric directions. Respiratory Opposite, so the cause is respiratory. The HCO₃⁻ of 24 is normal.

Step 3: The HCO₃⁻ is normal, so nothing is compensating yet.

Answer: uncompensated respiratory acidosis. Think slow breathing, an opioid overdose, or a sudden COPD flare.

Case 2: pH 7.25 · CO₂ 70 mmHg · HCO₃⁻ 30 mEq/L

Step 1: The pH of 7.25 is acidic.

Step 2: The CO₂ of 70 is high while the pH went down, so they moved in opposite directions. Respiratory Opposite, so the cause is respiratory. The HCO₃⁻ of 30 is high, which went the other way from the pH, so it is not the cause.

Step 3: The HCO₃⁻ is high, so the kidneys are trying to help. The pH is still under 7.35.

Answer: respiratory acidosis with partial metabolic compensation. This is the classic long-term COPD picture.

Case 3: pH 7.31 · CO₂ 30 mmHg · HCO₃⁻ 15 mEq/L

Step 1: The pH of 7.31 is acidic.

Step 2: The HCO₃⁻ of 15 is low and the pH is low too, so they moved in the same direction. Metabolic Equal, so the cause is metabolic. The CO₂ of 30 is low as well, which is the lungs blowing off acid.

Step 3: The CO₂ is low, so the lungs are breathing hard to help. The pH is still acidic.

Answer: metabolic acidosis with partial respiratory compensation. This is the classic DKA picture, with Kussmaul breathing.

Case 4: pH 7.48 · CO₂ 41 mmHg · HCO₃⁻ 29 mEq/L

Step 1: The pH of 7.48 is alkaline.

Step 2: The HCO₃⁻ of 29 is high and the pH is high too, so they moved in the same direction. Metabolic Equal, so the cause is metabolic. The CO₂ of 41 is normal.

Step 3: The CO₂ is normal, so the lungs have not started to compensate.

Answer: uncompensated metabolic alkalosis. Think heavy vomiting, NG suction, or too many antacids.

💡 Tic-tac-toe shortcut: Draw 3 columns and label them ACID, NORMAL, and BASE. Put each value (pH, CO₂, HCO₃⁻) in the right column. Two values in ACID means acidosis. The value sitting next to the pH tells you the type. One catch: CO₂ works backward from what you might guess. A high CO₂ is ACID. A low CO₂ is BASE. That is the same thing ROME says: the CO₂ and the pH move in opposite numeric directions.
⚠️ Common mix-up: Compensation does not push the pH past normal and out the other side. If the pH is normal but BOTH the CO₂ and the HCO₃⁻ are off, the picture is fully compensated. To find the first problem, see which side of 7.40 the pH sits on. Below 7.40 means the acidosis came first. Above 7.40 means the alkalosis came first.

❓ Free-Response Practice

  1. What does ROME stand for?
    Show answer
    Respiratory Opposite, Metabolic Equal.
  2. Read this one: pH 7.50, CO₂ 28 mmHg, HCO₃⁻ 22 mEq/L.
    Show answer
    The pH is alkaline. The CO₂ of 28 is low while the pH went up, so they moved in opposite directions. Respiratory Opposite points to the lungs. The HCO₃⁻ is normal. This is uncompensated respiratory alkalosis. Think fast breathing or a panic attack.
  3. Read this one: pH 7.32, CO₂ 35 mmHg, HCO₃⁻ 17 mEq/L.
    Show answer
    The pH is acidic. The CO₂ is normal. The HCO₃⁻ of 17 is low and the pH is low too, so Metabolic Equal points to the kidneys. This is uncompensated metabolic acidosis.
  4. Why does a high CO₂ act like an acid?
    Show answer
    CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻. More CO₂ drives that reaction forward, so the blood ends up with more H⁺.
  5. What does a normal pH with an abnormal CO₂ AND an abnormal HCO₃⁻ mean?
    Show answer
    It is fully compensated. The body pulled the pH back in range, but both systems are still off.

✅ Multiple Choice Practice

  1. pH 7.20, CO₂ 58 mmHg, HCO₃⁻ 22 mEq/L. This is:
    A) Uncompensated respiratory acidosis · B) Compensated metabolic acidosis · C) Metabolic alkalosis · D) Mixed disorder
    Show answer
    A. The pH is acidic and the CO₂ is high, so they moved in opposite directions. Respiratory Opposite points to the lungs. The HCO₃⁻ is normal, so nothing is compensating.
  2. pH 7.38, CO₂ 56 mmHg, HCO₃⁻ 32 mEq/L. This is:
    A) Uncompensated respiratory acidosis · B) Fully compensated respiratory acidosis · C) Metabolic alkalosis · D) Normal
    Show answer
    B. The pH is back in range but sits on the acid side of 7.40. Both the CO₂ and the HCO₃⁻ are off. That makes it fully compensated respiratory acidosis. This is the classic long-term COPD picture.
  3. A patient having a panic attack most likely has:
    A) Respiratory acidosis · B) Respiratory alkalosis · C) Metabolic acidosis · D) Metabolic alkalosis
    Show answer
    B. Fast breathing drops the CO₂, and that gives respiratory alkalosis.
🩺 Clinical Scenario
A 22-year-old with Type 1 diabetes comes in confused, with Kussmaul breathing and fruity breath. The ABG reads pH 7.18, CO₂ 22 mmHg, HCO₃⁻ 8 mEq/L. Read the gas and name the problem underneath it.
Show answer
The pH is very acidic. The CO₂ of 22 is very low, which is alkaline. The HCO₃⁻ of 8 is very low, which is acidic. The HCO₃⁻ and the pH both went down, so Metabolic Equal makes this a metabolic acidosis. The low CO₂ is the lungs compensating, which you see as Kussmaul breathing. The pH is still off, so this is metabolic acidosis with partial respiratory compensation. The cause underneath is DKA. Treatment is IV insulin, fluids, and potassium replacement.
☑ Self-Assessment Checklist
  • I can use the 3-step ABG method every time.
  • I can use ROME to tell a respiratory cause from a metabolic one.
  • I can tell uncompensated, partly compensated, and fully compensated apart.
  • I can read all 4 worked examples without looking.
  • I can match conditions like DKA, COPD, vomiting, and panic to their ABG patterns.
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TOPIC 7 🦠 Pathogens & Antibiotic Resistance MUST KNOW▼

Types of Pathogens

PathogenMain FeaturesExamples
BacteriaSingle cells. They can copy themselves on their ownStrep, Staph, TB, E. coli
VirusesThey run on the host cell's machinery. They cannot copy themselves aloneHIV, flu, COVID, herpes
FungiThey make spores. Some stay on the skin, some go deep into organsCandida (thrush, yeast), Tinea (ringworm)
ParasitesWorms (helminths), protozoa, and insects. They gain while the host losesMalaria, tapeworm, lice, scabies

Fungal Infections: Surface vs Deep

TypeWhereExamples
SuperficialMouth, skin, vaginaCandida (thrush, yeast infection), Tinea (ringworm)
DeepInside organs, which is a sign of a weak immune systemSystemic candidiasis, cryptococcal meningitis

Many fungi are normal flora, meaning they live on us all the time. They cause trouble when they overgrow or push into tissue. This often happens after antibiotics wipe out the bacteria that kept them in check.

Testing for Microbes

  • Gram stain (for bacteria):
    • Gram-positive bugs have a thick cell wall. They stain PURPLE.
    • Gram-negative bugs have a thin cell wall. They stain PINK or RED. They are harder to treat, because an outer membrane blocks drugs.
  • Culture and sensitivity. The culture names the bug. The sensitivity shows which antibiotic will work on it.

What Drives Antibiotic Resistance

  • Using antibiotics when they are not needed, like for a cold or the flu, which are viral.
  • Stopping the antibiotic early. The bacteria that live through it multiply and pass on resistance.
  • Heavy use on farms and in livestock.
  • Patients not taking the drug as directed.
  • Reaching for broad-spectrum antibiotics too often.
  • Picking up resistant bugs in the hospital, such as MRSA, VRE, and C. diff.
💡 Gram-stain trick: Positive = Purple. Negative stains pink or red, the opposite of purple. Gram-negative bugs are usually harder to treat, because their outer membrane keeps drugs out.
⚠️ Common mix-up: Antibiotics work ONLY on bacteria. They do nothing to viruses. Giving one for a cold or the flu feeds resistance and does not help the patient.

❓ Free-Response Practice

  1. List the 4 types of pathogens and one example of each.
    Show answer
    Bacteria, like E. coli. Viruses, like HIV. Fungi, like Candida. Parasites, like tapeworm.
  2. What color does a gram-positive bacterium stain, and why?
    Show answer
    Purple. Its thick cell wall holds on to the crystal violet dye.
  3. Why are gram-negative bacteria often harder to treat?
    Show answer
    Their outer membrane acts as a shield. It stops many antibiotics from reaching the target inside.
  4. List 3 things that drive antibiotic resistance.
    Show answer
    Using them when they are not needed, such as for a virus. Stopping the course early. Farm use. Reaching for broad-spectrum drugs too often. Patients not taking the drug as directed.
  5. What is the difference between a culture and a sensitivity?
    Show answer
    The culture names the bacteria. The sensitivity shows which antibiotic kills it.

✅ Multiple Choice Practice

  1. A patient has a fungal infection in the mouth. This is likely:
    A) Tinea · B) Candida (thrush) · C) Helminth · D) Virus
    Show answer
    B. Candida in the mouth is called thrush.
  2. Viruses differ from bacteria because viruses:
    A) Have a thick cell wall · B) Show up on a gram stain · C) Cannot copy themselves without a host cell · D) Are killed by antibiotics
    Show answer
    C. Viruses need a host cell to make more of themselves.
  3. Which of these feed antibiotic resistance? (SATA)
    A) Stopping antibiotics early · B) Using antibiotics for viral infections · C) Taking the drug as directed · D) Farm use of antibiotics · E) Hand washing
    Show answer
    A, B, D. Taking the drug as directed and washing hands both help PREVENT resistance.
🩺 Clinical Scenario
A patient finishes 10 days of a broad-spectrum antibiotic for pneumonia. Then the patient gets oral thrush and watery diarrhea. Explain what most likely happened.
Show answer
The antibiotic killed off the normal flora. That left room for other organisms to take over. Candida grew in the mouth, which is thrush. C. difficile may have grown in the gut, which causes the diarrhea. This is a classic problem after broad-spectrum antibiotics.
☑ Self-Assessment Checklist
  • I can name the 4 types of pathogens and an example of each.
  • I can read a gram stain. Positive is purple. Negative is pink and harder to treat.
  • I can list 3 things that drive antibiotic resistance.
  • I can tell a surface fungal infection from a deep one.
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TOPIC 8 🫕 Stages of Infection, Transmission, & TB MUST KNOW▼

Routes of Transmission

  • Direct contact means person to person, through touch or sex. Examples: HIV, herpes, scabies.
  • Indirect contact means through an object, called a fomite. Examples: doorknobs, IV poles.
  • Droplet means large drops from the airway that fall within about 3 to 6 feet. Examples: influenza, pertussis, meningococcal disease.
  • Airborne means tiny particles that float a long way. Examples: TB, measles, varicella. COVID spreads this way as well as by droplets, so do not file it under droplets alone.
  • Vector-borne means spread by an insect or animal. Examples: malaria from a mosquito, Lyme from a tick.
  • Vehicle or foodborne means through food or water that carries the bug.
  • Vertical means from mother to baby. It happens through the placenta, breast milk, or the birth canal.

Stages of Infection

StageWhat is Going OnSigns & Symptoms
1. ExposureThe pathogen gets into the bodyNone yet
2. IncubationThe pathogen multiplies. The person feels fineUsually no symptoms, but the person may already spread it
3. ProdromeThe first vague symptoms show upTired, low fever, feeling off. This stage spreads very easily
4. Acute (full)Symptoms peak. The immune system is working its hardestThe signs that point to this exact infection, like a rash or a cough
5. ConvalescentThe body clears the pathogen and healsSymptoms fade away bit by bit
6. ResolutionEither full recovery, or the infection settles in long-termNo symptoms, or symptoms that stay for the long run

Tuberculosis (TB)

TB is a bacterial infection caused by Mycobacterium tuberculosis. It usually sets up in the lungs. It spreads through the air, so it is airborne.

Latent TBActive TB
The immune system has walled the bacteria off. There are no symptoms. The person cannot pass it on. The skin test (PPD or TST) is positive, but the chest X-ray looks normal. The person feels well.The immune system has weakened, so TB breaks out of the wall. The person can pass it on. Signs include coughing up blood (hemoptysis), chest pain, a wet cough lasting over 3 weeks, fever, chills, weakness, tiredness, night sweats, and weight loss.
💡 Stages memory aid: "Every Infection Provides Acute Care Recovery." That gives you Exposure, Incubation, Prodrome, Acute, Convalescent, Resolution.
⚠️ Common mix-up: Latent TB means a positive test with NO symptoms, and the person cannot spread it. Active TB means symptoms AND the person can spread it. Both need treatment, but the drug plans are different.

❓ Free-Response Practice

  1. List the 6 stages of infection in order.
    Show answer
    Exposure → Incubation → Prodrome → Acute → Convalescent → Resolution.
  2. In which stage does a person usually spread the infection most?
    Show answer
    Prodrome. The symptoms are still vague, but the person is shedding a lot of the pathogen. Many people pass it on here without knowing.
  3. List 4 routes of spread with an example of each.
    Show answer
    Direct contact, like HIV. Droplet, like the flu. Airborne, like TB and measles. Vector-borne, like malaria from a mosquito. Food or water, like Salmonella. Vertical, like HIV passing from mother to baby.
  4. Compare latent TB with active TB.
    Show answer
    Latent TB is walled off by the immune system. There are no symptoms, the person cannot spread it, and the skin test is positive. In active TB the bacteria have escaped. There are symptoms, such as a cough over 3 weeks, coughing up blood, fever, and weight loss. The person can spread it.
  5. How does TB spread?
    Show answer
    Through the air, in tiny particles from the lungs.

✅ Multiple Choice Practice

  1. Which pathogen spreads through the air?
    A) HIV · B) Tuberculosis · C) Salmonella · D) Lyme
    Show answer
    B. TB spreads through the air.
  2. A patient with latent TB:
    A) Has active symptoms · B) Spreads it easily · C) Has a positive skin test but no symptoms · D) Should not be treated
    Show answer
    C. The PPD or TST is positive, there are no symptoms, and the person cannot spread it. We still treat it, to keep it from waking up.
  3. Vague tiredness and a low fever, before any specific symptoms, happen in which stage?
    A) Incubation · B) Prodrome · C) Acute · D) Resolution
    Show answer
    B. Prodrome is the stage of early, vague symptoms.
🩺 Clinical Scenario
A patient with HIV has had a wet cough for 4 weeks, night sweats, and blood in the sputum. The PPD is positive and the chest X-ray shows infiltrates. Why is this patient at higher risk for active TB?
Show answer
HIV weakens the immune system. It hits the CD4 T-helper cells hardest. Without those cells, the body cannot keep latent TB walled off. The bacteria break out and multiply, which gives active TB. Patients with weak immune systems should be screened often. Both latent and active TB need treatment right away.
☑ Self-Assessment Checklist
  • I can name the 6 stages of infection and put them in order.
  • I can name 5 routes of spread with examples.
  • I can tell latent TB from active TB and say how TB spreads.
  • I can list the classic TB symptoms.
↑ Back to top
TOPIC 9 🚰 UTIs: Cystitis vs. Pyelonephritis MUST KNOW▼
Acute Cystitis (bladder infection)Acute Pyelonephritis (kidney infection)
LocationThe bladder, which is the lower urinary tractThe kidney, which is the upper urinary tract
Local signsBurning with urination, going often, sudden urges, cloudy or bloody urineAll of those, plus flank pain
Whole-body signsNONE. There is usually no feverYES. Fever, feeling ill, nausea and vomiting
OnsetComes on slowlyComes on suddenly
ComplicationIt can travel up to the kidneys if untreatedUrosepsis can follow, which means bacteria in the blood
Lab findingsUrinalysis is positive, with WBCs, nitrites, and leukocyte esterase. The culture is positiveAll of those, plus a possibly high WBC count, positive blood cultures, and casts in the urine

How It Looks Different in Older Adults

Older adults often look nothing like the textbook picture:

  • Confusion, delirium, or any change in thinking may be the ONLY sign of a UTI.
  • They may have no burning and no need to go often.
  • Watch for falls, doing less than usual, and new loss of bladder control.
  • Always check for a UTI in an older patient with new confusion.

Risk Factors

  • Diabetes. Sugar in the urine feeds bacteria, and the immune system works less well.
  • HIV or any weak immune system.
  • Problems with the shape of the tract, such as kidney stones or urine flowing backward (vesicoureteral reflux).
  • Female anatomy. The urethra is shorter and sits closer to the anus.
  • A catheter left in place, which can cause a CAUTI.
  • Pregnancy.
  • Sex.
💡 Memory aid: Cystitis stays BELOW the belt, so you get bladder symptoms only. Pyelonephritis goes ABOVE the belt, so you get whole-body symptoms like fever and flank pain.
⚠️ Common mix-up: A confused older patient with no obvious UTI symptoms may still have one. Always run a urinalysis for new confusion in an older adult.

❓ Free-Response Practice

  1. List 3 symptoms of acute cystitis.
    Show answer
    Burning with urination, going often, sudden urges, and cloudy or bloody urine. There is usually NO fever.
  2. Which UTI usually brings fever and flank pain?
    Show answer
    Pyelonephritis, which is a kidney infection.
  3. How does an older patient with a UTI usually look?
    Show answer
    Confusion or any change in thinking may be the only sign. The classic burning and frequency may be missing.
  4. List 3 risk factors for a UTI.
    Show answer
    Diabetes. A weak immune system, such as from HIV. Problems with the shape of the tract. Female anatomy. A catheter. Pregnancy. Sex.
  5. What is urosepsis?
    Show answer
    A bloodstream infection that started in the urinary tract. It is what can happen when pyelonephritis goes untreated.

✅ Multiple Choice Practice

  1. The clearest thing that separates cystitis from pyelonephritis is:
    A) Burning with urination · B) Going often · C) Fever and flank pain · D) How clear the urine is
    Show answer
    C. Pyelonephritis adds whole-body symptoms: fever, flank pain, feeling ill, nausea and vomiting.
  2. Which of these are unusual UTI signs in an older adult? (SATA)
    A) New confusion · B) Falls · C) Classic burning with urination · D) New loss of bladder control · E) Bad flank pain
    Show answer
    A, B, D. Confusion, falls, and new loss of bladder control are the classic unusual signs.
  3. Untreated pyelonephritis can lead to:
    A) Otitis media · B) Urosepsis · C) Hepatitis · D) Hypothyroidism
    Show answer
    B. Urosepsis. Bacteria move from the kidney into the blood.
🩺 Clinical Scenario
An 82-year-old woman comes to the ER after a fall and for "acting strange." Vitals: T 38.2°C, HR 110, BP 96/58. Her WBC count is high. She says she has no pain. Name the most likely diagnosis and the first thing to check.
Show answer
Most likely a UTI, and possibly urosepsis. Older adults often show confusion and falls instead of burning with urination. The fever, fast heart rate, and low blood pressure all point toward sepsis. First steps: urinalysis, urine culture, blood cultures, IV fluids, and broad-spectrum antibiotics while the cultures run.
☑ Self-Assessment Checklist
  • I can list the local symptoms of cystitis.
  • I can describe the whole-body symptoms that mark pyelonephritis.
  • I can name the unusual ways a UTI shows up in older adults.
  • I can list 3 risk factors for a UTI.
  • I can say what urosepsis means.
↑ Back to top
TOPIC 10 🛡 Immunity, WBCs, & Immunoglobulins (GAMED) MUST KNOW▼

Innate vs Adaptive Immunity (the 3 Lines of Defense)

INNATE (1st & 2nd line)ADAPTIVE (3rd line)
SpeedActs fastTakes longer to get going
SpecificityWorks the same on everythingBuilt for one exact antigen
MemoryNo memoryHas memory, so it moves faster the next time
ComponentsBarriers like skin and mucus. Fluids like saliva, tears, and stomach acid. Macrophages and neutrophils. Inflammation and feverLymphocytes, which are B cells and T cells
Main jobBlock invaders and eat them fastAim at one target and make antibodies

Lymphocytes (Adaptive)

  • B cells make antibodies. Antibodies are also called immunoglobulins, and the five of them spell "GAMED."
  • T cells:
    • T helper cells (CD4) direct the B cells and the other T cells. Think of them as the conductor.
    • Cytotoxic T cells (CD8) kill infected cells and foreign cells themselves.

White Blood Cells (Leukocytes)

WBCWhat It Does
NeutrophilsThe most common WBC. FIRST on the scene in a bacterial infection. It eats invaders
LymphocytesB cells and T cells. They handle viruses and run adaptive immunity
Monocytes/MacrophagesThe "big eaters." They work in long infections and show antigens to T cells
EosinophilsParasites and allergies
BasophilsRelease histamine. They work in allergies

The 5 Immunoglobulins (Antibodies): GAMED

IgMain FeatureMemory Hook
IgGGives long-term immunity. Crosses the placenta from mom to baby. The most common one"LonG-term, Gestational"
IgASits in the fluids of mucous membranes, like saliva, tears, and breast milk. Blocks bugs at the door"Access · Alimentary canal"
IgMFirst one to show up. Found in body fluids. The largest antibody"Monitor · First Mover"
IgESits on mast cells. Works in allergies, inflammation, and parasites"AllergE"
IgDSits on B cells that have not met an antigen yet. Its job is less clear, but it helps switch B cells on"Don't know much about D"
💡 "GAMED" memory aids: G = Gestational and lonG-term · A = Alimentary and Access, so mucus · M = Monitor, the first one · E = AllergE · D = Don't know much.
⚠️ Common mix-up: Innate immunity is FAST and works on anything. Adaptive immunity is SLOW, picks one target, and REMEMBERS. Do not flip these around.

❓ Free-Response Practice

  1. Compare innate and adaptive immunity.
    Show answer
    Innate is fast, works on anything, and has no memory. It includes barriers, macrophages, and neutrophils. Adaptive is slower, aims at one target, and has memory. It uses B cells and T cells.
  2. Describe IgG, IgA, IgM, IgE, and IgD in one short phrase each.
    Show answer
    IgG: long-term, crosses the placenta. IgA: in mucus and other secretions. IgM: first to show up. IgE: allergies and parasites. IgD: on B cells that have not met an antigen.
  3. What do CD4 T helper cells do?
    Show answer
    They direct the immune response and keep B cells and T cells working together.
  4. Which WBC gets to a bacterial infection first?
    Show answer
    Neutrophil.
  5. Which WBC and which Ig take part in allergies?
    Show answer
    Eosinophils and basophils are the WBCs. IgE is the antibody, and it sits on mast cells.

✅ Multiple Choice Practice

  1. Which antibody crosses the placenta to protect a newborn?
    A) IgA · B) IgM · C) IgE · D) IgG
    Show answer
    D. IgG. Think "Gestational."
  2. The first antibody the body makes in a new infection is:
    A) IgG · B) IgA · C) IgM · D) IgE
    Show answer
    C. IgM. Think "Monitor," the first one there.
  3. Which of these belong to innate immunity? (SATA)
    A) Skin · B) IgG antibodies · C) Neutrophils · D) T helper cells · E) Stomach acid
    Show answer
    A, C, E. IgG and T helper cells belong to adaptive immunity.
🩺 Clinical Scenario
A mother who is breastfeeding gets a flu shot. How does that protect her and her newborn? Name the antibody and the kind of immunity the baby gets.
Show answer
The vaccine wakes up her adaptive immunity, and she makes antibodies against the flu, mostly IgG. During pregnancy, IgG already crossed the placenta to the baby. IgA in breast milk also guards the baby's mucous surfaces. The baby is not making any of these antibodies. The baby is borrowing mom's, and that is natural passive immunity.
☑ Self-Assessment Checklist
  • I can compare innate and adaptive immunity by speed, target, and memory.
  • I can name the main WBCs and what each one does.
  • I can name all 5 immunoglobulins (GAMED) and the main feature of each.
  • I can describe what CD4 T helper cells do.
↑ Back to top
TOPIC 11 ⚠️ Hypersensitivity, Anaphylaxis, Transplant & Immunity Types MUST KNOW▼

The 4 Types of Hypersensitivity Reactions

Hypersensitivity means the immune system over-reacts to an antigen. The body's own response does more harm to tissue than the antigen ever would.

TypeMain FeatureExamples
Type I, "Allergic"IgE sits on mast cells and triggers histamine release. It hits within minutes.Anaphylaxis, hay fever, asthma, food allergies, latex allergy
Type II, "antiBody"Antibodies (IgG, IgM) attack the body's own cellsTransfusion reaction from an ABO mismatch, hemolytic disease of the newborn, Goodpasture's
Type III, "Immune Complex"Antigen and antibody clump together and settle in tissueSLE (lupus), rheumatoid arthritis, glomerulonephritis
Type IV, "Delayed"T cells drive it. It takes hours to days.TB skin test (PPD), poison ivy, contact dermatitis, transplant rejection

Anaphylaxis, a Type I Emergency

IgE triggers a huge release of histamine. That leads to:

  • Skin: hives, flushing, and deep swelling called angioedema.
  • Lungs: wheezing, a harsh noise on breathing in (stridor), a tight throat, and a blocked airway.
  • Heart and vessels: low blood pressure, which is distributive shock, and a fast heart rate.
  • Gut: nausea, vomiting, and diarrhea.

Treatment: IM epinephrine comes first. Then oxygen, IV fluids, antihistamines, steroids, and airway support.

Transplant Rejection

TypeWhen It HappensCause
HyperacuteMinutes to hoursAntibodies the patient already had (Type II), often an ABO mismatch
AcuteDays to monthsT cells drive it (Type IV). This is the most common kind. It is treated with immunosuppressant drugs
ChronicMonths to yearsSeveral mechanisms mixed together. The organ is damaged slowly

Graft-versus-host disease (GVHD) works the OTHER way. Here the donor's T cells attack the person who got the graft. It shows up mostly after bone marrow or stem cell transplants.

Types of Immunity, and How You Get Each

TypeHow You Get ItExample
Natural ActiveYour body makes antibodies after you get sickCatching chickenpox leaves you immune for life
Artificial ActiveYour body makes antibodies after a vaccineFlu shot, MMR, COVID vaccine
Natural PassiveAntibodies pass from mom to babyIgG across the placenta, IgA in breast milk
Artificial PassiveYou receive someone else's antibodiesIVIG, rabies or Hep B shots after exposure, monoclonal antibody infusions
💡 Immunity memory aid: "Active = you Actively make the antibodies." "Passive = Pre-made antibodies handed to you." Active lasts a long time. Passive only guards you for a while.
⚠️ Common mix-up: A TB skin test (PPD) is a Type IV, delayed reaction, NOT Type I. It takes 48 to 72 hours to show up.

❓ Free-Response Practice

  1. List the 4 types of hypersensitivity with one example each.
    Show answer
    Type I is Allergic, like anaphylaxis. Type II is antiBody, like an ABO transfusion reaction. Type III is Immune complex, like SLE. Type IV is Delayed, like a PPD, poison ivy, or transplant rejection.
  2. What are the main signs of anaphylaxis?
    Show answer
    Hives and angioedema. Wheezing, stridor, and a tight airway. Low blood pressure with a fast heart rate. Nausea, vomiting, and diarrhea. The first drug is IM epinephrine.
  3. What causes hyperacute transplant rejection?
    Show answer
    Antibodies the patient already had, which is a Type II reaction. It is often an ABO mismatch. It hits within minutes to hours of the transplant.
  4. Compare the 4 ways to get immunity.
    Show answer
    Natural active means you caught the disease. Artificial active means you got a vaccine. Natural passive means you got mom's antibodies, through the placenta or breast milk. Artificial passive means you were given an antibody product, like IVIG or a monoclonal antibody.
  5. Why does passive immunity wear off so fast?
    Show answer
    The body is not making those antibodies itself. The borrowed ones break down over weeks to months, and no memory cells get built.

✅ Multiple Choice Practice

  1. A bee sting causes throat swelling and low blood pressure. Which type of reaction is this?
    A) Type I · B) Type II · C) Type III · D) Type IV
    Show answer
    A. Type I. IgE drives it, it hits right away, and this is anaphylaxis.
  2. A patient gets mismatched blood, then has fever, back pain, and bloody urine. This is:
    A) Type I · B) Type II · C) Type III · D) Type IV
    Show answer
    B. Type II. Antibodies break down the donor red cells, which is a hemolytic transfusion reaction.
  3. Getting a tetanus vaccine gives you which type of immunity?
    A) Natural active · B) Artificial active · C) Natural passive · D) Artificial passive
    Show answer
    B. Artificial active. Your own body makes the antibodies after the shot.
🩺 Clinical Scenario
A patient gets a kidney transplant. Within 6 hours the new kidney is failing. ABO testing shows a mismatch. Which type of hypersensitivity is this? What is this rejection timing called? What immune step is to blame?
Show answer
This is Type II hypersensitivity, driven by antibodies. The rejection is called hyperacute. The patient already had anti-A or anti-B antibodies. Those antibodies latch onto the donor kidney cells and switch on complement. The kidney is destroyed fast. This is why ABO typing and crossmatching must happen BEFORE a transplant.
☑ Self-Assessment Checklist
  • I can name the 4 types of hypersensitivity with examples.
  • I can describe the signs of anaphylaxis and the first drug to give.
  • I can compare hyperacute, acute, and chronic transplant rejection.
  • I can match the 4 types of immunity to how you get each one.
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TOPIC 12 🧴 HIV/AIDS, Immunodeficiency, Autoimmunity & Blood Cancers MUST KNOW▼

HIV & AIDS

HIV (Human Immunodeficiency Virus) is a retrovirus. It attacks CD4 T helper cells, the cells that conduct the immune response.

  • As the CD4 count falls, the immune system loses its conductor and stops working together.
  • AIDS is the late stage. It means a CD4 count under 200, or an infection that only takes hold in AIDS.

Infections That Take Hold in AIDS

SystemExamples
RespiratoryTB, PCP (Pneumocystis pneumonia)
GIThrush in the mouth (Candida), and Candida in the esophagus
CNSToxoplasmosis, cryptococcal meningitis
CancersKaposi sarcoma, non-Hodgkin lymphoma

Immunodeficiency: What Causes It

  • Cancer, and cancer treatment such as chemo and radiation.
  • HIV infection.
  • Diabetes. Neutrophils work poorly, and high sugar feeds organisms.
  • Long-term stress. Steady cortisol holds the immune system down.
  • Poor nutrition.
  • Having the spleen removed, since it is a key immune organ.
  • Drugs that hold the immune system down, used after transplants and in autoimmune disease.
  • Being very young or very old.

Autoimmune Disease vs Immunodeficiency

AutoimmuneImmunodeficiency
ProblemThe immune system attacks the person's own bodyThe immune system is too weak to fight infection
Risk factorsRuns in families. More common in women than menHIV, chemo, diabetes, spleen removal, poor nutrition
ExamplesLupus (SLE), RA, MS, Type 1 diabetes, Graves' diseaseAIDS, SCID, transplant patients on immunosuppressant drugs

Leukemia (Cancer of the WBCs)

Leukemia is cancer of young blood cells. The cells multiply out of control, and they do not do their job.

  • Lymphoblastic leukemias hit the cells that would become lymphocytes, meaning B and T cells.
  • Myelocytic leukemias hit the cells that would become basophils, eosinophils, and neutrophils.
  • Acute means it starts fast, the cells stay immature, and it moves hard.
  • Chronic means it starts slowly, the cells are more mature, and it runs longer.

All leukemias share these signs: tiredness, anemia, infections, bleeding and bruising, weight loss, and a big spleen (splenomegaly).

Lymphoma: Hodgkin vs Non-Hodgkin

Hodgkin LymphomaNon-Hodgkin Lymphoma
Where it isIn one area. It spreads node to neighboring nodeSpread out. It skips around
Telltale cellReed-Sternberg cellsNo Reed-Sternberg cells
Outside the lymph nodesNot oftenOften
AgeYounger adults and adolescentsOlder adults
OutlookBetter, with a high survival rate. It is caught early, stays in one area, and responds well to treatmentWorse
💡 Hodgkin = "Has Reed-Sternberg, High survival." Non-Hodgkin has nO Reed-Sternberg, spreads wider, hits older patients, and has a worse outlook.
⚠️ Common mix-up: AIDS means a CD4 count under 200, OR an infection that only takes hold in AIDS. Just having HIV is not AIDS. A person can carry HIV for years and never reach AIDS, especially on antiretroviral drugs.

❓ Free-Response Practice

  1. Which cell does HIV attack, and why does that hurt the immune system so much?
    Show answer
    It attacks CD4 T helper cells. Those cells run the whole adaptive immune response. Without them, B cells and the other T cells cannot work right.
  2. Define AIDS.
    Show answer
    Late HIV with a CD4 count under 200 cells/mm³, OR an infection that only takes hold in AIDS.
  3. List 4 causes of a weak immune system.
    Show answer
    Cancer or chemo. HIV. Diabetes. Poor nutrition. Long-term stress. Spleen removal. Drugs that hold the immune system down.
  4. Which cell tells Hodgkin lymphoma apart from non-Hodgkin lymphoma?
    Show answer
    The Reed-Sternberg cell, which shows up in Hodgkin.
  5. Why does Hodgkin lymphoma have a better outlook?
    Show answer
    It stays in one area and spreads node to node, so it gets caught earlier. It hits younger patients, who handle treatment better. It also responds strongly to chemo and radiation.

✅ Multiple Choice Practice

  1. HIV is a:
    A) DNA virus · B) Retrovirus · C) Bacteria · D) Fungus
    Show answer
    B. A retrovirus. It uses reverse transcriptase to slip its genes into the host's DNA.
  2. Reed-Sternberg cells point to:
    A) Acute leukemia · B) Hodgkin lymphoma · C) Non-Hodgkin lymphoma · D) Kaposi sarcoma
    Show answer
    B. Hodgkin lymphoma.
  3. Which of these are AIDS-defining illnesses? (SATA)
    A) Common cold · B) Kaposi sarcoma · C) PCP pneumonia · D) Thrush in the mouth · E) Strep throat
    Show answer
    B, C. Kaposi sarcoma and PCP are AIDS-defining. Thrush in the mouth is common with a weak immune system, but on its own it is not AIDS-defining.
🩺 Clinical Scenario
A 35-year-old with untreated HIV comes in short of breath. The CD4 count is 95, and the chest X-ray shows spread-out infiltrates. The sputum grows Pneumocystis jirovecii. Why did this patient get PCP? What is the diagnosis now?
Show answer
A CD4 count under 200 leaves the patient unable to fight off infections like Pneumocystis (PCP). A CD4 under 200 plus an AIDS-defining infection like PCP means this patient has moved from HIV to AIDS. Treatment: start antiretroviral therapy, treat the PCP with TMP-SMX, and keep the patient on preventive drugs going forward.
☑ Self-Assessment Checklist
  • I can say what HIV attacks (CD4) and define AIDS.
  • I can name the common infections that take hold in AIDS.
  • I can list 4 or more causes of a weak immune system.
  • I can compare autoimmune disease with a weak immune system.
  • I can compare lymphoblastic and myelocytic leukemias, and Hodgkin with non-Hodgkin lymphoma.
↑ Back to top

🎯 Rapid-Review Cheat Sheet

ABG Normals
pH 7.35–7.45 · CO₂ 35–45 mmHg · HCO₃⁻ 22–26 mEq/L · PaO₂ 80–100 mmHg
Electrolyte Normals
Na 135–145 mEq/L · K 3.5–5.0 mEq/L · Ca 8.5–10.5 mg/dL · P 2.5–4.5 mg/dL · Mg 1.5–2.5 mEq/L
ROME Trick
Respiratory Opposite, Metabolic Equal
Buffer Speeds
Serum (seconds) → Respiratory (minutes) → Renal (days, STRONGEST)
RAAS Trigger
Low BP, volume, or sodium → renin → angiotensin II → tight vessels + aldosterone + ADH + thirst
ANP/BNP
The mirror image of RAAS. They dump Na and water. A high BNP points to heart failure.
K⁺ & pH
Acidosis raises K⁺. Alkalosis lowers K⁺.
EKG Changes
High K = peaked T waves. Low K = flat T waves plus U waves.
Edema Causes
↑ hydrostatic, ↓ oncotic (low albumin), blocked lymph vessels, leaky capillaries
Stages of Infection
Exposure → Incubation → Prodrome → Acute → Convalescent → Resolution
Gram Stain
Positive = PURPLE (thick wall). Negative = PINK (thin wall, harder to treat).
TB
Airborne. Latent means a positive PPD with no symptoms. Active spreads, with a cough over 3 weeks and blood in the sputum.
UTIs
Cystitis is the bladder, with no fever. Pyelonephritis is the kidney, with fever and flank pain. In older adults, look for confusion.
Immunity (Innate vs Adaptive)
Innate is fast with no memory. Adaptive is slow and remembers, using B and T cells.
GAMED (Ig)
G = lonG-term and placenta. A = mucus and other secretions. M = first one there. E = allergE and mast cells. D = B cells that have not met an antigen.
Hypersensitivity
I = Allergic, IgE. II = antiBody, like a transfusion reaction. III = Immune complex, like SLE. IV = Delayed, like PPD and poison ivy.
HIV/AIDS
HIV attacks CD4 T helper cells. AIDS means CD4 under 200, OR an AIDS-defining infection.
Lymphoma
Hodgkin has Reed-Sternberg cells, stays local, hits younger patients, and has a BETTER outlook. Non-Hodgkin spreads wide, hits older patients, and is worse.
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📚 Quick Glossary

Fluids & Hormones
  • ICF / ECF: inside cells, which is high in K⁺, and outside cells, which is high in Na⁺.
  • Hydrostatic pressure: the pushing force from blood.
  • Oncotic pressure: the pulling force from albumin.
  • Edema: fluid in the tissues. It comes from a pressure imbalance, a blocked lymph vessel, or leaky capillaries.
  • RAAS: renin → angiotensin II → aldosterone. It raises BP.
  • Aldosterone: takes back Na and water, and dumps K.
  • ADH: takes back water only.
  • ANP / BNP: the mirror image of RAAS. They dump Na and water.
Electrolytes
  • Hyponatremia / Hypernatremia: both hit the brain, bringing confusion and seizures.
  • Hypokalemia / Hyperkalemia: both cause odd heart rhythms, with EKG changes.
  • Hypocalcemia: Trousseau's sign, Chvostek's sign, and tetany.
  • Hypercalcemia: "bones, stones, groans, psychic moans."
  • Trousseau's sign: a hand spasm when the BP cuff inflates.
  • Chvostek's sign: a face twitch when you tap the cheek.
Acid-Base & ABGs
  • Acidosis: pH under 7.35. Alkalosis: pH over 7.45.
  • CO₂ = acid. HCO₃⁻ = base.
  • Kussmaul respirations: deep, fast breathing, seen in DKA.
  • Buffer systems: serum, respiratory, and renal.
  • Anion gap: wide in DKA, lactic acidosis, and salicylate poisoning.
  • Compensation: the OTHER value shifts to pull the pH back toward normal.
Pathogens & Infection
  • Gram positive: thick wall, stains purple. Gram negative: thin wall, stains pink, harder to treat.
  • Antibiotic resistance: grows from misuse, unfinished courses, and farm use.
  • TB latent vs active: walled off vs spreading. Only active TB passes to others.
  • Stages of infection: Exposure → Incubation → Prodrome → Acute → Convalescent → Resolution.
  • Cystitis: a bladder infection, with no fever. Pyelonephritis: a kidney infection, with fever and flank pain.
  • Urosepsis: a bloodstream infection that started as a UTI.
Immune System
  • Innate: fast, works on anything, no memory. Adaptive: slow, picks one target, remembers.
  • B cells: make antibodies. T cells: CD4 helpers and CD8 killers.
  • WBCs: neutrophils, lymphocytes, monocytes, eosinophils, and basophils.
  • Immunoglobulins (GAMED): G is long-term, A guards mucus surfaces, M is first there, E drives allergy, D sits on B cells that have not met an antigen.
  • Hypersensitivity I–IV: allergic, antiBody, immune complex, and delayed.
  • Anaphylaxis: Type I. Treat it with IM epinephrine.
  • Immunity types: natural or artificial, crossed with active or passive.
Immune Disorders & Cancers
  • HIV: a retrovirus that attacks CD4 cells.
  • AIDS: CD4 under 200, or an AIDS-defining infection.
  • Opportunistic infections: PCP, thrush in the mouth, toxoplasmosis, and Kaposi sarcoma.
  • Autoimmune: the immune system attacks the body itself, as in lupus, RA, and Type 1 DM.
  • Immunodeficiency: the immune system is too weak, as in HIV, chemo, poor nutrition, and spleen removal.
  • Leukemia: cancer of young white blood cells. It is either lymphoblastic (B and T) or myelocytic.
  • Hodgkin lymphoma: has Reed-Sternberg cells, stays local, and has a better outlook.
  • Non-Hodgkin lymphoma: spreads wide, has no Reed-Sternberg cells, hits older patients, and is worse.

🎯 Final Study Tips for Exam 1

  • Learn the lab values first. If you do not know the normal ranges, you cannot spot an abnormal pattern.
  • Practice ABGs until they feel automatic. Work all 4 examples, then write your own.
  • Build a one-page table with each electrolyte and its high and low signs side by side. Then write it again without looking.
  • Tie each mechanism to its signs. Do not just memorize lists. Understand WHY high K peaks the T waves, and WHY low calcium causes tetany.
  • Practice with the hidden answers. Pulling an answer from memory beats rereading every time.
  • Use the cheat sheet for a last pass before you self-test.
  • Do not rush. There are 50 questions and plenty of time. Read every option. A select-all item needs ALL the right answers.
💾 To save this guide as a PDF to study offline:
In your browser, press Ctrl+P on Windows or Cmd+P on a Mac. Choose "Save as PDF." Every closed topic opens by itself, so the printed copy is complete.
✨ You've got this. Modules 1 and 2 hold a lot, but the patterns are learnable. Trust the work. ✨
Pathophysiology · a study guide by Dr. Akash Garg