EXAM 2 PATHO

3 Layers of the Heart:

Pericardium: fibrous covering around heart; physical infection protection

Myocardium: Muscle; A & V

Endocardium: lines heart & valves

Diastole Cycle Steps:

1. Early: V. relaxes; semilunar cloves → AV valve opens → V. filled w/blood

2. Mid: A. & V. relaxed; continued blood filling

3. Late: SA nodes contract → A. contracts → V. + blood → AV node

Systole Steps:

1. AV node → Purkinje + ventricular cells → V. contracts

2. AV valve closes → Semilunar opens → blood (V. → arteries)

Preload & Afterload:

• Volume of blood stretching V. muscles at end of diastole

• Psi/tension L.V. generates to push blood → aorta; systematic + pulmonary resistance

  • ^ = ^ Cardiac overload

Cardiac Contractility:

Heart change its contraction force

• Inotropic drugs: influences cardiac contraction force

HR:

Regulates CO

• Chronotropic drugs: effects HR control; can increase (+) or decrease (-)

CO & Stroke Volume:

CO: SV x HR

• 3.5-8 L/min

Stroke Volume: 50-100 ml/beat

Tests for Cardiovascular Function

Assessment:

• Pulse= bounding & high= good psi

• Capillary refill

• Auscultate

Radiology: Size & contour of heart & structures

• Chest X-ray

• CT scan

• MRI

Stress Testing:

• Treadmill

• Thallium & Cardiolite scans

ECG: HR & rhythm

• Electrical activity

Echocardiogram:

• US

• Anatomic structures + functions

• Ejection Fraction: 50-70% of blood pushed via L.V.

Cardiac Cathererization:

• Fluoroscopy → light up vessels

Atherosclerosis:

fat deposit in the arteries; plaque buildup in lumen

• Leading cause of coronary artery & cerebrovascular disease

• Coronary arteries → blocked → heart ischemia → MI

• Legs, carotid, brain

• Based on atherosclerosis

Arteriosclerosis:

less elastic and stretchable

• Thickening + hardening of vessel walls

Artery Layers:

Intima: endothelium

Media: smooth & elastic tissue

Externa: Connective tissue

Ischemia from Atherosclerosis:

v O2 → Pain

Depend on which tissues affected + how long it lasts

• Angina (Stable/Unstable)

• Claudication: PVD

• Subsequent thrombosis from unstable plaques → ischemia, infarction, stroke

Lipoproteins:

Water-soluble phospholipids & apoproteins

Transport ↓↓↓

• Cholesterol & Triglycerides:

  • Hydrophobic, insoluble

• for energy utilization, lipid deposition, steroid hormone, bile acid formation

Lipoproteins Density:

more protein = ^ density

more lipid (triglycerides) = v density

Types: 

• Chylomicrons

• VLDL: carries large triglycerides #

• IDL

• LDL: carries cholesterol

• HDL: 50% protein

Atherosclerosis steps:

1. Endothelial (intima) Cell Injury

• HTN, smoking, hyperlipidemia, toxins, viruses, immune reactions, stress, hyperhomocystenimia

2. Migration of Inflammatory Cells and Formation of Fatty streak

• From LDL entering inside → phagocytes eat LDL → foam cells formation → Fatty streak

3. Fibrous plaque (Fibrous Cap)

• SMC

• Fibroblasts

• Ca

• Elastin

• Endothelium

4. Complicated lesion

• Stable → platelets add up to “help” → thrombus (platelet + fibrin) → unstable plaque → angina

Atherosclerosis:

D/x:

• pulses, bruits, check tissue perfusion

• Doppler, angiography

T/x:

• smoking cessation, lowering cholesterol

• Restoring blood flow

• Catheterization

Thrombus:

blood clot remaining and attached in vessel wall

Thromboembolism

detached thrombus

Embolism:

obstruction of vessel by embolus

• Bolus of matter circulating in blood stream

• Blood clot, fat, air

Aneurysm:

localized dilation of vessel/cardiac chamber

• weakened artery via stretches

• Ruptures & hemorrhage

• clot formation

Hypertension:

90-95%: idiopathic; primary hypertension

5-10%: identifiable etiologic cause; secondary hypertension

HTN Risk Factors

Family history

Advanced age.

Smoking

Obesity

Heavy alcohol consumption.

Gender (Male < 50 years, Female > 50 years)

Black race - higher renin producers-

High dietary sodium intake

Low dietary intake of potassium, magnesium, and calcium

Insulin resistance/glucose intolerance

Primary Hypertension

95% of cases of HTN

Unknown cause

Is usually of gradual onset

Peak age: 30-50

Asymptomatic for 10 to 20 years

Triggers include obesity, psychological stress, high-sodium intake, and alcohol intake over I ounce per day

Secondary Hypertension

Refers to sustained increases in blood pressure that result from identifiable underlying systemic diseases

Renal Vascular Disease

decreased flow to the kidney results in persistent increases in RAAS activity

Renal Parenchyma Disease

⚫ damage to glomeruli or tubules leads to increased RAAS activity

Adrenocortical Tumors

⚫ increased production of cortisol and mineralocorticoids (aldosterone) lead to sodium retention and potassium loss

Adrenomedullary tumors (non cancerous) (pheochromocytoma)

⚫ increased production of catecholamines with dramatic increases in heart rate and peripheral resistance

Check for tumor on adrenal gland

Secondary Hypertension Manifestations:

No symptoms till heart, brain, kidneys vascular changes

• Brain → CVA, TIA

• Retina → Blindness

• Heart → MI

• Kidneys → Proteinuria, edema, renal failure

Lifestyle changes for HTN:

• Weight v

• DASH diet

• Sodium v

• aerobic physical activity

• Moderate alcohol consumption

Meds for HTN:

“First line”

• Thiazide-type diuretics

• Calcium Channel Blockers (CCBs)

• Working with RAAS:

  • Angiotensin-converting enzyme inhibitors (ACEIs)

  • Angiotensin II receptor blocking agents (ARBs)

Later line meds for HTN:

Beta-blockers (BBs)

Alpha-blockers

Vasodilating BBs (nebivolol)

Direct vasodilators (hydralazine)

Loop diuretics

Aldosterone antagonists

Cultural changes in med administration for HTN:

Orthostatic/Postural HTN:

v sys & dia psi when standing

• >20/>10

s/s: Dizziness, blurred vision, syncope

Causes: meds, prolonged immobility, starvation, exhausted

Heart failure (CHF):

Inability of heart to pump blood to meet needs

• Right sided: inability of RV to provide enough blood → pulmonary circulation; from LHF

• Left sided (LHF): inability of LV to produce enough stroke volume → v CO → blood backs into lungs; from HTN 

Systole vs Diastolic CHF:

Sys: ventricles cannot empty properly; v muscle ability to contract

Dia: ventricles fail to fill properly

CHF Causes::

Primary: Defective malfunction

• Cardiomyopathy

• Coronary heart disease (CAD)

• Valvular disorders

Secondary:

• HTN → LHF

• Renal failure

• Pulmonary Disease → RHF

• Anemia

CHF risk factors:

• CAD

• HTN

• ^ Cholesterol

• Age

• Smoking

• Obese

• Proteinuria

• Diabetes

LHF vs RHF:

LHF:

1. shortness of breath

2. Difficulty breathing

3. Wheezing

4. Pink frothy/ blood sputum

5. v urine output

RHF:

• Swollen ankles & feet → Edema

• Hepatosplenomegaly

• Weight gain

• Abdominal pain

• JVD

• Nocturia

CHF compensation:

Ventricular dilation

Hypertrophy

^ Sympathetic N.S.

RAAS cascade

In the end, these mechanisms are gonna make the heart work harder → CHF worse

CHF compensation diagram

CHF diagnosis:

CXR

ECHO

EKG

Blood work

• Electrolytes

• Serum osmolarity

• BNP

CHF t/x:

Improve pumping

• Ionotropics

• Lowering preload

  • Diuretics

• Lowering after load:

  • ACEI, ARBs, aldosterone inhibitors

Peripheral Vascular Disease (PVD)

PAD

Vein disease

Claudication: PAD, low O2 → ischemia, plaque formation

• intermitent: only when pt walks feels pain

• Severe: pain anytime

PAD:

Atherosclorosis

Thromboangiitis

Raynnud Phenomenon Disease

Thromboangiitis/ Buerger Disease

Inflammatory Disease of peripheral arteries of hands & feet

• Young men that smoke

s/s:

• Pain, tenderness, gangrenes, malformed nails

t/x: stop smoking bro

Raynud Phenomenon:

Vasospasm of small arteries/oles in fingers & feet (less common)

• cold environments

s/s: ischemia

• Numb, tingling, rubor, gangrene

Vein Disease:

Varicose Veins

DVT

Chronic Venous Insufficiency

Varicose Veins:

veins in which blood has pooled → distended, palpable veins; open vein valves

Causes:

• Trauma

• Clots

• Gradual Venous distention: from standing

Chronic Venous Insufficiencies:

Inadequate venous return; worse than Varicose & DVTs

s/s: pooling of blood in veins in lower extremity edema

• LE circulation becomes sluggish

• Necrosis from venous stasis ulcers

DVT:

s/s: pain to site, warm to touch

risk factors: 

• Circulatory stasis

• Vascular wall injury

• Hypercoagulable state

  • Pregnancy

  • Surgery

  • Estrogen Therapy

d/x: doppler

t/x: anticoagulants

• Heparin

• Enoxaparin

(TPA dissolves thrombus)

Coronary Artery Disease (CAD):

Plaques; chest pain from low O2

CAD risk factors:

Dyslipidemia

HTN

Smoke

Diabetes

Obesity

Sedentary

CAD d/x:

Ischemic disease → dyspnea

MI → syncope, dyspnea, nause

Resting EKG

CAD t/x:

Life long care

Angioplasty & bypass surgery not a cure
Reducing risk factors

Percutaneous transluminal coronary angioplasty

Drugs

• Antiplatelts

• Statins → v cholesterol

Coronary Bypass Surgery

Angina:

chest pain from reduced blood flow to heart

CAD symptom

• Prinzmetal: from vasospasms of vessels; no atherosclerosis

• Stable: ischemia during exercise

  • Nitroglycerin → dilates arteries → less pain

• Unstable: complicated plaque; pain at rest

• MI: necrosis; prolonged ischemia in myocardium

  • STEMI (elevated ST) or non

Angina Steps

Stable Plaques:

Thick fibrous cap

Partially blocked vessels

No clots/emboli

Unstable Plaques:

Thin Fibrous caps

Rupture & form blood clots:

• Thrombosis

• Embolization

Ischemia, Scars, MI:

lack of oxygen

20-40 mins = cell death

__________________

Scars replace muscle but loses function

__________________

Hypertrophy → loss of contractility

• MI remodeling

MI manifestations:

Bad pain

• Referred

• Tightness

• 15-20 mins

• nor relieved by NTG & rest

Tachycardia/pnea & Dyspnea

Diaphoresis

Elderly, women, diabetes: atypical presentation of MI

Feeling of impending doom

EKG changes:

Ischemia: inverted T wave & ST depression

Injury, MI: ST elevated

Q wave formation (infarction/necrosis)

Cardiac Biomakers:

Enzymes released by heart when damaged (Myocyte Necrosis)

• Myoglobin

• CK-MB: detected after 2-3 hrs

• Troponin I & T: detected after 3-4 hours

• Creatine Kinase

bold means its specific to MN

MI diagnosis:

Blood work for Biomarkers, electrolytes (K), blood gases

EKG, CXR, ECHO, stress test

MI t/x:

O2

Meds:

• Antianginals: Nitrates

• Antiplatelet: ASA, aspirin

• Analgesics

• Thrombolytics

• Antiarrhythmics

Heart Wall Disorders

Disorders of the Pericardium

• Acute pericarditis

• Pericardial effusion - tamponade

• Constrictive pericarditis

Disorders of the Myocardium

• Cardiomyopathies

Disorders of the Endocardium

• Valvular dysfunctions

• Acute rheumatic fever

• Infective endocarditis

Acute Pericarditis:

Inflamed and roughened

• 90% from viruses

• Bacteria

• Autoimmune diseases

s/s:

• Chest Pain worsening w/ respirations or movement

• When lying down

• Dysphagia

• Restlessness

D/x:

• Friction rub

• Sinus Tachycardia

• Low grade fever

• Echocardiogram

Complications: 

• Hypotension

• Pulse paradoxus: v BP when inspirating (deep breath)

  • Normal drop is 10

  • Abnormal is 20 mmHg

t/x:

• NSAIDs

Pericardial effusion:

Fluid accumulation in cavity

• Serous effusion

• Serosanguineous

• Blood

Leads to Cardiac Tamponade:

Cardiac Temponde:

Fluid/blood in pericardial sac compresses heart

• from trauma, Mi, med, bleeding

s/s:

• Muffled heart sounds

• BECK’s triad: low arterial BP and distended neck veins

d/x:

• ECHO, CT, chest

t/x:

• Pericardial window

• Pericar

Cardiomyopathy:

Myocardium

three types:

• Dilated: Dilated heart → big floppy heart → unable to pump

• Hypertrophic: thickening of myocardium

• Restrictive: cannot fill diastolic the heart with blood; heart is ridged 

Valvular Defects:

Stenosis: valve does not open all the way; harder to force blood out → narrow

Regurgitation: valve does not close all the way → leaks 

Mitral Valve Prolapse:

Congenitive Disease; mitral valve cups billow upward → LA during systole

• Women

• Asymptomatic

• Heart Murmurs

• Prevent Infective Endocarditis

Infective Endocarditis:

May include 1+ valves

• Bacteria infection most common

Risk factors: IV drug uses, Valvular heart disease

s/s:

• Fever

• Infection signs

• Murmurs

• Lesions

• Micro embolism

d/x:

• Blood cultures

• ECHO

t/x:

• Antibiotics

• Valve replacement

Rheumatic Heart Disease:

Rheumatic fever: inflammatory diseases affecting heart, joints, skin, brain, valves

• Group A streptococcal throat infection

Risk Factors: Sore throat, H/A, fever, abd. pain, swollen pain

T/x: ABX, fever

EKG:

• P wave → Atrial depolarization (atria activated → contract).

• PR interval → Signal travels through AV node → to ventricles.

• QRS complex → Ventricular depolarization (ventricles activated → contract).

  • Atrial repolarization happens here too, but it’s hidden inside the QRS.

• ST segment → Early part of ventricular repolarization (should be flat).

• T wave → Ventricular repolarization (ventricles reset/relax).

• U wave (sometimes seen) → Final phase of ventricular repolarization (extra reset, not always visible).

Electrical pathway of the heart:

1. Sinoatrial node

2. AV node: connects between A. & V.; impulse is slowed → allow atria to contract & empty blood before stimulating the ventricles → depolarization 

3. Bundle of his

4. Bundle Branches

5. Purkinje Fibers

Mechanical Activity:

Must have electrical impulse

• Muscle contraction + pulse

• “Lub Dub” → S1 & S2

  • S1: close AV valve

  • S2: close Seminular valves

Electrical Activity:

Prepares heart for contraction

• Precedes mechanical activity

• Not always followed by mechanical activity

• EKG/ECG

PACEMAKERS:

SA: 60-100 bts/min

AV: “back up” 40-60 bts/min

Ventricular cells: back up too; 20-45 bts/min

EKG Paper

Horizontal:

• Small box - 0.04 s

• Large box - 0.2 s

Vertically:

• Large box - 0.5 mV

Every 3 seconds (15 large boxes) marked by a vertical line; 60 seconds would be 90 HR

Helps when calculating HR

Determining PR interval:

Normal: 0.12-0.2 secs

• (3-5 small boxes)

• If 4 small boxes = 0.16 secs

QRS duration:

Normal: 0.04-0.12 secs

• (1-3 small boxes)

• If 2 small boxes = 0.08 secs

Normal Sinus Rhythm (NSR):

Electrical impulse formed in SA node & conducted normally

• Arrhythmias if irregular

Dysrhythmia Formation:

Arise from:

• Sinus mode

• Atrial Cells

• AV junction

  • Ventricular cells

SA node problems:

fire too slow → Sinus Bradycardia

fire too fast → Sinus Tachycardia

Sinus Bradycardia:

<60 bpm

regular

Normal P wavers

Normal PR & QRS

Sinus Tachycardia":

>100 bpm; from stress

regular

Normal P wavers

Normal PR & QRS

Atrial cells problem:

Atrial Flutter

Atrial Fibrillation

Atrial Flutter:

fires continuously due to a looping re-entrant pathway; makes F (flutter) waves 250-350 bpm

• Only some impulses conducted through AV node

• W/every 2nd, 3rd, 4th impulse → QRS → AV node

• Irregular P waves, No PR interval, (QRS, regularity, rate) normal

Atrial Fibrillation

No organized atrial depolarization → no normal P wave; not originating from sinus node

• Chaotic atrial activity → irregular rate

• 2-4%

• 8-10% in pt older than 80 yrs

• No P waves & PR intervals, irregular

• Rate, QRS normal

Ventricular cell problems:

Ventricular Tachycardia

Ventricular Fibrillation

Ventricular Tachycardia

fire continuously due to looping re-entrant pathways in ventricles (most common)

• can create or not create pulse at times

• Faster rate, no P waves & PR, wide (>0.12) QRS

• Regular

Ventricular Fibrillation

COMPLETETLY ABNORMAL; NO PULSE → CPR; from multiple foci

• No rate, irregular, no P & PR, wide & irrecognizable QRS

ST elevation:

J point is higher; elevated ST segment

ST elevation infarction:

Normal EKG → Ischemia → ST depression → Infarction → ST elevation

• Depression: peaked T waves → T inversion

• Elevation: Q waves appearance

Innate/Natural Immunity:

nonspecific; rapid

• Only to group of microbes

• Phagocytes, nk, dendritic cells

• Monocytes → macrophages

1st line:

1. Skin

2. Mucous

3. Flora (stomach, i.s.)

2nd line:

1. Innate immune cells

2. Inflammation *

3. Complement

4. Antimicrobials

Adaptive/Acquired Immunity:

specific; slower

• for each unique antigen

3rd line:

• Lymphocytes

1. B cells

2. T cells vvv

• Helper & Killer t cells

B Lymphocytes:

Memory cells: efficient; antibody response to subsequent antigen recognition

Plasma: Secretes antibodies/iG

T Lymphocytes:

Cytotoxic T cells: specific cellular antigen destruction

Helper T cells: Activates antigen-specific T cells

Mucus & Cilia:

lysozymes → destroy bacteria cell wall

• moves mucus out to keep antigens out

Inflammatory Response:

2nd line; from many problems

• Trauma, infection, chemical injury, foreign bodies, ischemia

• s/s: Redness, swelling, heat, pain, function loss

WBCs abundance

Neutrophils > Lymphocytes > Monocytes > Eosinophils > Basophils

“Never let monkeys eat bananas”

Leukocytes (WBCs):

• Granulocytes: N, E, B

• Monocytes → Macrophages & Dendritic

  • Initiate adaptive response

  • Dendrites turn on lymphocytes

• NK cells, lymphocytes

• Mast cells: histamine; located in tissues

  • Allergies, asthma, inflammation

Neutrophils:

Most abundant granulocytes (55% WBC)

• Early responder of innate immunity