Patho Exam 3

Heart Diagram

Aorta

• Brachiocephalic artery, Right subclavian artery, right common carotid artery

• Left common carotid artery

• Left subclavian artery

Tricuspid → Mitral Valve

Wiggers Diagram

1 - All 4 relaxed

2 - Atria contract; ventricles fill

3 - Ventricular Systole begins

3a - Isovolumetric contraction, up the hill

3b- Ventricular ejection

4- Blood against semilunar valves closure, blood flows into relaxed atria; dicrotic notch

5 - Late ventricular diastole - Isovolumetric relaxation

AV Closure (Tricuspid and Mitral Valves)

S1, Lub

Semilunar (Pulmonary and Aortic) closer

S2,/Dub, Ventricular diastole begins 2/3

Preload

Amount of blood in ventricle is full

LV = 5-12

Optimal action (most effective)

Excessive stretch ↓ venous return

Less optimal stretch → ↓ preload, SV, and CO

Afterload SVR

Resistant blood flow out of the ventricle

Systemic Vascular Resistance 800- 1,400

Inotropy/Contractility

Ventricular

Negative - hypoxic cells, lower ATP

Positive - increased calcium

SV

Stroke Volume: blood amount ventricular ejection

EF

Ejection Fraction (55-75%)

CO

Blood pumped/minute

HR x SV = 4- 6 L/min at rest, 8 if active/healthy

Cardiac Index (CI)

Adjusted, body surface area: 2.5–4.0

HR

Frequency of left ventricular contractions = 60–100

Tachycardia shortens diastole, reducing ventricular filling

Increased HR =

Lower Ventricle fill, Lower SV, Lower CO

BP = CO x SVR

CO 4-6, up to 8

SVR 800-1,400

Circulatory System

Pulmonary: R heart → Pulmonary artery → Lungs → Pulmonary veins (large, thin, elastic) → L heart | low pressure 25/10 mean is 15

Systemic - L heart → Aorta → Organs/tissues (nutrients/wastes in blood/cells→ Vena Cava → R heart

Blood vessels layers

Tunica intima: Endothelial cells

Tunica media: Smooth muscle, elastic tissue, diameter

Tunica externa (adventitia): Connective tissue, collagen support & strength

Arteries/Capillary Network

Away from the heart

Arterioles: Small branches of arteries; smooth muscle regulates blood flow

Metarterioles: Connect arterioles to capillaries; regulate blood flow

Capillaries: Thin endothelial layer (tunica intima); exchange of fluids, nutrients, gases, and wastes between the blood and interstitial space (ISS).

Veins

Return blood to the heart; thin, less muscle/elasticity

Venous valves: Prevent backflow in from the limbs (none in head & neck)

Venules: Small vessels, capillary beds, carry it into larger veins, very thin

Blood Pressure

Systolic <120

Diastolic <80

Pulse Pressure

Systolic - diastolic = 40

Mean arterial Pressure (MAP)

Tissue blood flow

(S+ (D2) / 3 = 70-110

Dyslipidemia

Primary (Familial) Hypercholesterolemia: >LDL cholesterol → tissues, tendons, cornea.

Heterozygous: One gene; LDL = 190–400 mg/dL.

Homozygous: Two genes; LDL = 400–1,000+ mg/dL.

Optimal: <100 mg/dL

Very high: >190 mg/dL

Secondary Hyperlipidemia - Lifestyle, diet, obesity, T2DM, families with similar lifestyles

Blood Lipids

Cholesterol - Waxy, fat-like substance; cell membranes + phospholipid

75% - body, 25%- food

Desirable: <200 mg/dL,

High cholesterol: >240 mg/dL

Triglycerides - Stored body fat, energy reserve

Normal: <150 mg/dL

High: 200–499 mg/dL

Very high: >500 mg/dL

Chylomicrons - Large lipoprotein carrier for these two

Lipoprotein’s (carry fat through the blood)

LDL Cholesterol → body tissues.

Optimal: <100 mg/dL

Very high: >190 mg/dL

HDL Cholesterol → liver/removal.

Low: <40 men, <50 women, Protective: >60

VLDL - Triglycerides from the liver → body tissues

Acute Arterial Occlusion & Peripheral artery disease

Acute Arterial Occlusion - An embolus breaks off, travels through the bloodstream, and blocks another vessel. Sudden, severe pain, pallor, pulselessness, paresthesia, and paralysis. Emergency

Peripheral Artery Disease (PAD) - Reduced arterial blood flow to the extremities; intermittent claudication: Calf pain, cool hairless skin, decreased pulse, poor wound healing, rubor

Raynaud disease

Vasospasm, arteries, cold, females, pale/white, number fingers, avoid triggers

Atheroscleoris

Chronic Inflammatory disease; buildup of lipid-rich plaques in arterial walls/intima; Stable or unstable, elevated LDL and VLDL cholesterol

• Damage to the endothelium occurs (initial step); vascular inflammation; lipids and inflammatory cells diffuse into the endothelium, releasing growth factors; smooth muscle proliferation; artery becomes changed or distorted; released cytokines cause the accumulation of monocytes and other WBCs

• Elevated levels of serum cholesterol LDL-C overwhelm healthy endothelium, abnormal endothelial metabolism

Causes CAD

Prevent/treat: heart-healthy diet, exercise, and statins

1. Fatty streaks: Flat, yellow lipid deposits (child)

2. Fibrous plaque: Raised, grayish-white plaque that thickens/narrow the arterial wall

3. Thrombosis: A blood clot forms when a plaque ruptures or erodes, potentially blocking blood flow to the heart or brain → MI or ischemic stroke.

Stable plaque: Thicker fibrous/calcified cap and smaller lipid core; less likely to rupture

Vulnerable/unstable plaque: Thin cap, larger lipid core, inflammation. Rupture, thrombus formation, UA or MI.

High-Sensitivity C-Reactive Protein (hs-CRP)

Chronic systemic inflammation contributes to CAD + MI

<1 low risk >3 high risk >10 test again infection

Homocysteine

Amino acids damage the endothelial lining

Eat B6, B12, and B2 (riboflavin)

Ankle Branchial Index (ABI)

Highest (Systolic) ankle BP

Highest arm BP

= 1.0-1.4

Severe PAD <0.5

HTN

Hypertensive Crisis/Emergency: Severe increase, acute organ damage, or stroke

White Coat Hypertension: BP is elevated in a clinical setting but normal at home

Primary Hypertension: High BP, no cause

Secondary Hypertension: another condition → medications, kidney disease, or RAAS dysfunction. Increases systemic vascular resistance (SVR) and afterload.

• May be asymptomatic until organ damage occurs. Patients may have difficulty adhering to medications because the effects are not immediately noticeable.

Normal <120/<80

Elevated: 120-129/<80

Stage 1: 130-139/80-89

Stage 2: >140/>90

Goal

18-59 <140/90

80+ <150/90

Aneurysms

Aortic Aneurysm (Dilation/Pouch): Weak & bulging of the aortic wall (Atherosclerosis risk)

• Abdominal Aortic Aneurysm: asymptomatic; abdominal pain. Rupture risk: >4 cm

• Ascending Aortic Aneurysm: May cause chest/back pain, hoarseness, swollen face

Aortic Dissection: A tear in the inner aortic wall (enlargement or rupture) - False Aneurysms

Pathway of Conduction

1) SA node

2) Atrial depolarization (P wave)

3) Atrioventricular (AV) node

4) Bundle of His

5) Right and left bundle branches

6) Purkinje fibers

Ventricular depolarization (QRS complex) >0.12 seconds

PR interval: From the beginning of the P wave to the beginning of the QRS complex. Normal: 0.12–0.20 seconds (3–5 small boxes).

Dysrhythmias

Atrial flutter: Sawtooth-shaped flutter (F) waves.

Atrial fibrillation: No distinct, organized P waves

Ventricular tachycardia (VT): Up-and-down QRS complexes

Asystole: No activity; confirm with another lead & check the monitor connections

Cardiomyopathies (Heart muscle disease)

Hypertrophic cardiomyopathy: Genetic; thickens and stiffens, left ventricular filling. treat: beta/calcium channel blockers

Dilated cardiomyopathy: Common + transplant. Ventricles enlarge = reduced EF, systolic dysfunction

Restrictive cardiomyopathy: Uncommon, ventricles become stiff, can’t relax or fill

Takotsubo (stress-induced) cardiomyopathy: broken-heart syndrome, women post-menopause. Stress; only acute complications

Infective Endocarditis (IE)

Heart valve regurgitation (Staphylococcus aureus)

Risk factors: Prosthetic heart valves, previous endocarditis, congenital heart disease, implanted cardiac devices, and injection drugs

B — Blood cultures

E — Echocardiographic

T — Temperature >38/100.4

O — Osler nodes tender

M — Murmur/micro evidence

E — Embolic phenomena + emergency

Rheumatic Heart Disease

Disease post-group A streptococcal throat infection

Heart effects: Inflammation can cause mitral valve regurgitation/stenosis

Features: Fever, polyarthritis, and carditis. Aschoff bodies

Treatment note: Aspirin relieve symptoms, but not the underlining

Valve Disorders

Aortic stenosis: Left ventricular outflow; murmur radiating to carotids.

Aortic regurgitation: Blood flows back into LV during diastole; high-pitched, diastolic decrescendo murmur.

Mitral stenosis: Narrow mitral opening impairs LV filling during diastole; atrial fibrillation may occur; diastolic rumble & snap.

Mitral regurgitation: Blood leaks back into the left atrium during systole; holosystolic murmur at the apex, radiating to the axilla.

Heart Failure (HF)

The heart can’t meet the body’s needs, leading to dyspnea, fatigue, and fluid retention.

HFrEF (reduced), systolic HF: LVEF <40%; end-systolic volume rises, the ventricle dilates, and SV falls.

Left-sided backup: pulmonary congestion

Right-sided backup: peripheral edema (diuretic therapy)

HFpEF (preserved), diastolic HF: LVEF >50%; elevated filling pressures; the ventricle is stiff

HFmrEF (Mildly reduced) LVEF 41–49%;

Pericardium

Two-layer sac around the heart; protects, stable, barrier to infection, reduces friction, lubricates

15–50 mL of fluid

Pericarditis

Inflammation of the thin pericardial sac; fibrin-rich inflammation, viral or idiopathic: pericardium may thicken (men) Acute <4-6 weeks, Chronic >3 months

Radiating chest pain (tripod position), ECG, friction rub

WideST elevation, PR depression

Inflammation increases Erythrocyte sedimentation rate (ESR)

Pericardial Effusion

• Fluid in the pericardial space → inflammation, infection, or cancer

• Slow accumulation = no symptoms

• Rapid accumulation = tamponade (Squeeze, water-bottle sign, emergency)

• Echocardiography identifies

• Chronic effusion: water-bottle-shaped

Cardiac tamponade

Emergency

Fluid in the pericardial sac limits diastolic filling → collapse or arrest.

Tachycardia, swinging heart, water bottle sign, large effusion

Urgent drainage: image-guided pericardiocentesis or a subxiphoid approach.

Signs: Beck’s triad: JVD, Narrowed pulse pressure, Muffled heart sounds

Constrictive Pericarditis

Fibrous fluid, calcified scar tissue, and a thickened pericardium restrict ventricular expansion & diastolic filling, reducing SV and CO

Findings include fatigue, peripheral/pedal edema, ascites, and venous congestion as blood backs up into the systemic veins

Angina

Stable: Predictable pressure, squeezing, or tightness with exertion or stress; relieved by rest or nitroglycerin

Unstable (UA): New or worsening chest pain; ischemia without a rise in cardiac troponin, indicating no acute myocardial injury. ECG normal or ST depression; emergency.

Vasospastic (Prinzmetal) Angina

Transient coronary spasms, @rest or at night; ST elevation; dysrhythmias; not MI

Acute coronary syndrome

Reduction in myocardial blood flow

Stable, unstable, variant angina, NSTEMI, and STEMI

Chest discomfort + SOB

Coronary Artery Disease

Reduced blood flow through the coronary arteries (atherosclerosis, angina, MI, etc.)

Left coronary circulation flow is about 225 mL/min.

Myocardial Infarction

Unstable angina: ischemia without detectable myocardial necrosis

Troponin: protein released when heart muscle cells are injured NSTEMI + STEMI

NSTEMI: myocardial infarction without qualifying ST elevation. subendocardial

STEMI: myocardial infarction with qualifying ST elevation; emergency, transmural

PCI hospital: Blood flow within 90 minutes; 120+ minutes → Fibrinolysis for eligible STEMI patients

Necrotic myocardium → scar. Ventricular septal or free-wall rupture may occur 3–7 days later

Sudden cardiac death: rapid symptoms within 1 hour.

Endocrine Glands

Exocrine: Ducts, surface, secretory; not part of the endocrine system.

Endocrine: Ductless; secrete specific hormones (Chemical messengers) into the bloodstream. Hormones bind to receptors to be delivered to body tissues and organs.

Pancreas and Liver have both

Endocrine & Thyroid glands

Hypothalamus: “Master switchboard” controls the endocrine system. It secretes hormones to anterior pituitary. TRH stimulates the anterior pituitary to secrete TSH, which stimulates the thyroid gland to produce and release thyroid hormones (T3 and T4)

Thalamus → Hypothalamus (pea-sized) → pituitary gland

Pituitary gland: “Master gland” controls the functions of many target glands and cells.

Anterior pituitary: FLAT PG — FSH, LH, ACTH, TSH, prolactin, and GH.

Posterior pituitary: ADH and oxytocin

Thyroid Gland: Two lobes + TH storage

TRH → TSH → T3 and T4 → bone growth, heart function, and metabolism. (Negative feedback)

Serum Osmolality at 265, the body stops vasopressin, what will happen?

More urine is excreted; serum will increase

Parathyroid Glands

Blood calcium/phosphate homeostasis

Stops osteoblast activity (forms new bone) and osteoclast activity (breaks down old bone).

Low serum Ca²⁺ → Increases PTH release, raising calcium by promoting bone breakdown (Osteoclast)

High serum Ca²⁺ → Decreases PTH release, reducing calcium by building bone (Osteoblast)

Thymus

• Behind the sternum, Immune & T cells before birth/childhood

• After puberty, the thymus decreases in size and is gradually replaced with fatty tissue

Adrenal glands

Above renal/kidney, regulates stress

Aldosterone - sodium and water reabsorption and potassium excretion

Cortisol - glucocorticoid; increases BG & appetite; high levels → insulin resistance, diabetes, depression, anxiety, and weight gain

Epinephrine - acute stress

Norepinephrine - potent/strong vasoconstriction

Pancreas: Exocrine vs. Endocrine Function

Exocrine/Ducts: 99%; digestive enzymes

Endocrine/Bloodstream: 1%; hormones & insulin 18–40 units/day or 0.5–1 unit/hour

Gonads: Ovaries and testes.

Endocrine tissues: heart releases atrial natriuretic peptide (ANP) → diuresis in the kidneys → release renin.

Release of Hormones

Steady-state release: (TH) Steady rate; blood hormone levels fluctuate very little

Intermittent release: (GH) Large amounts only as needed

Cyclic release: Fluctuates in a recurring cycle (Estrogen)

Diurnal release: Time of day → Cortisol higher (7–8 AM) & lower (2–4 AM).

Growth Hormone

Endocrine disorders can change personal appearance

GHs: GH, TH, insulin, and androgens/sex hormones

Linear bone growth in kids GH 2nd half of night

Short stature is defined as a height below 3% of population

Familial/constitutional short stature are variations (not disease)

TH bound to

globulin = inactive

Free T3 or T4 hormones, not protein-bound, enter target cells/active.

Hyperthyriodism

Excessive TH: women, smoking, iodine deficiency or excess

Graves Disease – common, autoimmune; TSH increases thyroid hormone (TH); hypertension (HTN), goiter, ophthalmopathy/exophthalmos (bulging eyes), hypermetabolic. Treatment: Radioactive iodine, beta blockers for symptoms.

Thyroid Storm – Rare, life-threatening, triggered by stress or trauma, high fever, tachycardia, agitation, psychosis, emergency. Treatment: Stabilize hemodynamic/circulatory status, then aggressively treat everything

Hypothyriodism

Shortage of dietary iodine

Goiter - 1st visible sign

Hashimoto’s Thyroiditis – Autoimmune, iodine normal, most common cause in the US. Everything slow, more menstrual bleeding, anemia.

Postpartum Thyroiditis – Inflammation after giving birth, often undiagnosed. First - hyperthyroidism. Second - 4–8 months later, the thyroid has lost most of its hormones; lasts 6–12 months, hypothyroidism. More likely permanent hypothyroidism within 5–10 years.

Manifestations of Hypothyroidism – Weakness, fatigue, weight gain, cold intolerance. Babies/Cretinism: jaundice, umbilical hernia, and sleepiness. Maternal iodine deficiency: impaired growth and intellectual disability.

Myxedema – Rare, non-pitting, mucus-type edema of the shins, feet, and eyes.

Myxedema Coma – Life-threatening; hypothyroidism in every cell → IV TH

Adrenal Cortical Insuffiency

Addison Disease – Adrenal insufficiency, hypocortisolism (everything low) low aldosterone (helps retain sodium and water), sodium and water loss, Lifelong hormone replacement therapy, medical alert bracelet

Cushing Syndrome – Excessive amounts of glucocorticoids (hypercortisolism): obesity, moon face, delayed healing, high blood sugar, infections. Treatment: Stop excessive steroid use, remove tumor surgically, radiation.

DM test

Hyperglycemia → inability to transport glucose into cells, breakdown of fats and proteins.

Blood Tests

Fasting Plasma Glucose (FPG): Morning, 8 hours of fasting; 80–100 normal, >126 DM.

Random Plasma Glucose: >200 DM.

Oral Glucose Tolerance Test (OGTT): 75 g of concentrated glucose, 2 hours later; <40 mg/dL normal, >200 DM

Capillary Whole Blood Glucose Monitoring

Hemoglobin A1C: Glucose molecules become irreversibly bound to the hemoglobin. A1C: 120-day RBC lifespan. No fasting required. <5.7% is good; >6.5% DM

Goal: DM should keep A1C <7%

Urine Test: Renal tubular maximum is approximately 180, the kidneys can no longer reabsorb all the glucose

Prediabetes

Blood glucose is elevated but does not meet the criteria for DM. Early treatment → diet, exercise, and weight loss of 7% of body weight. Exercise 30 mins/day x 5 days

T1DM

• Autoimmune: insulin-producing pancreatic beta cells within the islets of Langerhans.

• Ketosis and ketoacidosis

• Dependent on exogenous insulin to live; rarely diagnosed <9, peaks around 12

• High BG greater than 180 mg/dL and breakdown of body fats and proteins

• Glucagon (opposite of insulin) a high BG level fails to suppress the production of glucagon, further increasing hyperglycemia.

• Polyuria, polydipsia, polyphagia, weight loss.

Latent diabetes

Subtype of T1DM, adulthood, genetic, T1.5DM still produces some insulin for the first 6 months, age 35+, autoantibodies present against islet beta cells

T2DM

Chronic, persistent hyperglycemia; insulin supply is insufficient to meet needs; 45+ abdominal obesity & PCOS; insulin levels are high, low, or normal.

Treatment: Diet and exercise; aerobic activity 90–150 minutes per week, metformin first-line, goal A1C <7%.

Insulin Resistance (Metabolic Syndrome)

Excess body fat (T2DM), insulin resistance impair glucose regulation, compensatory increase in beta-cell → hyperinsulinemia

Maturity-Onset Diabetes of the Young (MODY)

Autosomal dominant inheritance (single-gene mutation), family history of DM (T2DM)

Gestational Diabetes

• Glucose intolerance during pregnancy

• Oral glucose drink, BG 2 hours later, larger babies, higher risk of fetal abnormalities.

Chronic Complications of Diabetes

• Neuropathy: loss of sensation; high blood sugar damages nerves over time

• Vascular: microangiopathy, thickening/hardening of capillaries/small arteries, strokes, heart attacks

• Infections: bacteria thrive in high-glucose states.

• Claudication, gangrene, amputation

T1DM Acute Life-Threatening Complication

Diabetic Ketoacidosis – Hyperglycemia, increased ketone concentration, blood glucose (BG) of 400–800 mg/dL, Kussmaul respirations and lethargy

Give Insulin, low Na+ & Cl-, high K+, dehydration NS 2 L over 1-1.5hrs

Hyperosmolar Hyperglycemic State (HHS)

Elderly T2DM w/ infection, MI, or stroke, CHOs, neurological deficits (not common)

Hypoglycemia

Low blood glucose <70: anxiety/irritability/hangry

Subcutaneous (SubQ) insulin can cause

Apple, grape, or cranberry juice; no orange juice if kidney disease 15/15 rule

Numbers to Memorize

Left Ventricle Preload: 5-12

Systemic Vascular Resistance: 800-1,400

Ejection Fraction: 55-75%

CO: 4-6 8 active/healthy

Cardiac Index: 2.5-4

Pulmonary low pressure: 25/10 mean 15

Blood Pressure: <120/<80

Pulse Pressure: 40

Mean arterial Pressure S + (2D) / 3 = 70-110

Heterozygous Primary: 190-400

Homozygous Primary: 400-1,000+

LDL: 100-190

Cholesterol: 200-240

Triglycerides 150-500

HDL: 40 Men, 50 Women, 60 Protective

High-sensitivity C-reactive Protein: <1 low risk >3 high risk >10 test again infection

Ankle Branchial Index: 1.0-1.4 normal, <0.5 Severe PAD

Heart Failure: r <40, p >50, mr 41-49

Pericardium: 15-50

Left coronary circulation flow is about 225 mL/min

Anterior pituitary: FLAT PG: FSH, LH, ACTH, TSH, Prolactin, and GH

Short Stature - below 3%

Fasting BG >126

Infective Endocarditis: BE TOME Blood cultures, echocardiographic, temp >38/100.4, oslet nodes tender, Murmur/micro evidence, embolic phenomena, emergency

Coarctation of the aorta

Physical Defects (Coarctation of the Aorta): A congenital condition where the aortic arch is narrowed, increasing systemic vascular resistance (SVR) and afterload. This creates a major resistance to forward blood flow.