Exam 2 Patho

Define the four stages of hemostasis.

Vasoconstriction platelet plug formation coagulation cascade activation fibrin clot formation (then clot retraction/dissolution).

What triggers the intrinsic coagulation pathway?

Contact activation by exposed endothelial collagen; measured by PTT.

What triggers the extrinsic coagulation pathway?

Tissue factor release from damaged endothelium; measured by PT.

Why is vitamin K important in coagulation?

Needed for gamma-carboxylation of clotting factors II, VII, IX, X; deficiency prolongs PT/INR.

Describe the 'common pathway' in coagulation.

Factors X prothrombin (II) thrombin fibrinogen fibrin to form stable clot.

Name two natural anticoagulants.

Protein C and Protein S (also antithrombin III).

How does liver disease affect coagulation?

Decreases synthesis of clotting factors and clotting proteins, leading to bleeding risk.

Clinical significance of prolonged PTT vs prolonged PT?

Prolonged PTT suggests intrinsic pathway problem or heparin effect; prolonged PT suggests extrinsic pathway problem or warfarin effect.

Define thrombocytopenia and a common cause.

Platelets <150,000/µL; causes include decreased production (aplastic anemia), increased destruction (immune), or sequestration (splenomegaly).

Key clinical signs of thrombocytopenia.

Petechiae, purpura, mucosal bleeding, easy bruising, prolonged bleeding from cuts.

What is DIC in one sentence?

A systemic, uncontrolled activation of coagulation causing widespread microthrombi and paradoxical bleeding due to consumption of clotting factors.

Name three common triggers of DIC.

Sepsis (especially gram-negative), obstetric complications, severe trauma/major transfusion.

Why do patients with DIC both clot and bleed?

Massive thrombin generation consumes platelets and clotting factors microthrombi + later bleeding from factor depletion.

Immediate nursing priority for suspected DIC?

Recognize bleeding/clotting signs, notify physician, support organ perfusion, prepare for blood product replacement as ordered.

Primary difference between iron deficiency and B12 deficiency anemia.

Iron deficiency = microcytic, no neurologic signs; B12 deficiency = macrocytic (megaloblastic) with neurologic deficits due to demyelination.

Common causes of iron deficiency anemia.

Dietary deficiency, chronic blood loss (GI bleeding), increased demands (pregnancy, growth).

Key neurologic signs of B12 deficiency.

Paresthesias, loss of vibration/position sense, spastic ataxia, cognitive changes.

What lab finding suggests iron deficiency anemia?

Low hemoglobin/hematocrit, low MCV (microcytosis), low ferritin, high TIBC.

Define primary vs secondary polycythemia.

Primary: myeloproliferative neoplasm increasing all cell lines (e.g., polycythemia vera). Secondary: increased EPO from hypoxia or tumors, mainly raises RBCs.

Why is polycythemia dangerous?

Increased blood viscosity thrombosis risk, impaired tissue perfusion, hypertension.

Define neutropenia and the ANC threshold with high infection risk.

Neutropenia is low neutrophils; ANC <500/µL confers high risk of serious infection.

Major causes of aplastic anemia.

Autoimmune destruction of marrow, radiation/chemicals (benzene), drugs (chloramphenicol), viral infections.

Typical clinical triad in aplastic anemia.

Pancytopenia: anemia (fatigue), leukopenia (infections), thrombocytopenia (bleeding).

Where do B and T lymphocytes mature?

B cells mature in bone marrow; T cells mature in thymus.

What is the pathophysiology of infectious mononucleosis (Mono)?

EBV infects B cells atypical lymphocyte proliferation and lymphadenopathy; virus remains latent in B cells.

Key complication to watch for in mono?

Splenic enlargement risk of splenic rupture; avoid contact sports.

Difference between Hodgkin and Non-Hodgkin lymphoma in one line.

Hodgkin: Reed-Sternberg cells present, often localized; Non-Hodgkin: diverse B/T cell origins, more diffuse spread.

What chromosomal abnormality is associated with CML?

Philadelphia chromosome (t(9;22)) creating BCR-ABL fusion protein.

Acute vs chronic leukemia-presentation difference.

Acute: rapid onset, blasts, cytopenias; Chronic: slower, mature-appearing cells, may be asymptomatic initially.

Multiple myeloma classic features (CRABBI).

HyperCalcemia, Renal failure, Anemia, Bone lesions, Bone pain, Infections (immunoglobulin dysfunction).

Nursing implication for hematologic malignancies.

Monitor for infection, bleeding, anemia; educate about treatment side effects and infection precautions.

List major causes of atherosclerosis.

Dyslipidemia (^LDL, vHDL), smoking, hypertension, diabetes, obesity, family history.

Brief pathogenesis of atherosclerotic plaque formation.

Endothelial injury LDL infiltration macrophage foam cells fatty streak fibrous plaque possible rupture.

Clinical consequences of plaque rupture.

Thrombus formation acute vessel occlusion MI, stroke, limb ischemia.

Differentiate primary vs secondary dyslipidemia in one line.

Primary = genetic lipid metabolism defects; Secondary = lifestyle, diseases, or meds.

What are xanthomas?

Cholesterol deposits in tendons/skin indicating lipid disorders.

Define aneurysm and a key risk for AAA.

Localized arterial dilation; major risk: atherosclerosis and smoking (esp. for abdominal aortic aneurysm).

Difference between true and false (pseudo) aneurysm.

True involves all vessel wall layers; false is a vessel wall tear with extravascular hematoma.

Classic symptom of thoracic aortic aneurysm.

Chest/back/neck pain, possible hoarseness or dysphagia from mass effect.

Pathophysiology of aortic dissection in one sentence.

Intimal tear allows blood to enter medial layer, creating a false lumen and rapid propagation of dissection.

Classic pain description for aortic dissection.

Sudden, severe 'tearing' or 'ripping' chest/back pain.

Explain 6 P's of acute arterial occlusion.

Pallor, Pain, Pulselessness, Paresthesia, Paralysis, Polar (cold) - signals limb ischemia.

Most common cardiac source of arterial emboli.

Atrial fibrillation causing left atrial thrombus.

How does peripheral artery disease present?

Intermittent claudication (exercise-induced calf pain), cool extremities, poor wound healing.

Why can plaques cause aneurysms?

Plaque-associated inflammation and wall weakening can lead to dilation and aneurysm formation.

Treatment priority for ruptured aortic aneurysm.

Immediate surgical repair and hemorrhage control-life-threatening emergency.

Role of LDL in atherosclerosis.

Enters intima and becomes oxidized taken up by macrophages forming foam cells.

Nursing focus for acute arterial occlusion.

Rapid recognition of 6 P's, notify provider, maintain limb position, prepare for reperfusion interventions.

What is Virchow's triad?

Stasis, endothelial injury, and hypercoagulability-factors that predispose to venous thrombosis.

Clinical signs of DVT.

Unilateral leg pain, swelling, warmth, and calf tenderness; may be asymptomatic.

Pathophysiology of chronic venous insufficiency leading to stasis ulcers.

Persistent venous hypertension capillary leakage, skin pigmentation, poor nutrition stasis dermatitis and ulcers.

Primary vs secondary hypertension in one line.

Primary: no single cause (multifactorial); Secondary: due to identifiable cause (renal disease, endocrine).

How does hypertension cause target-organ damage?

Sustained high pressure injures endothelium and arterioles ischemia/damage in heart, brain, kidney, eyes.

Define orthostatic hypotension diagnostic drop.

Decrease in systolic BP ≥20 mmHg or diastolic ≥10 mmHg upon standing with symptoms.

Underlying pathophysiology of CAD in one line.

Atherosclerotic plaque narrows coronary arteries reducing myocardial blood supply.

Difference between stable angina and unstable angina.

Stable: predictable exertional chest pain from fixed stenosis; Unstable: new/worsening/rest pain from plaque rupture/partial occlusion.

Define NSTEMI vs STEMI quickly.

NSTEMI: myocardial necrosis without ST elevation (partial occlusion); STEMI: transmural infarct with ST elevation from complete occlusion.

Role of troponin in ACS diagnosis.

Troponin is highly specific marker of myocardial injury, rises within ~3 hours and remains elevated for days.

ECG sign of transmural myocardial injury.

ST-segment elevation in leads corresponding to affected territory.

Primary mechanism of thrombosis after plaque rupture.

Exposure of tissue factor and subendothelial collagen platelet adhesion/aggregation and thrombin generation.

Typical presentation of MI in women/older adults.

Atypical symptoms-shortness of breath, fatigue, nausea rather than classic chest pain.

Why 'time is muscle' in MI?

Longer occlusion more irreversible myocardial necrosis and worse functional loss.

Initial emergency management priorities for suspected STEMI.

Activate reperfusion (PCI or thrombolytics if PCI unavailable), MONA-B as per protocols, continuous monitoring.

Difference between white and red thrombi.

White: platelet-rich, associated with unstable angina; Red: fibrin/RBC-rich, cause complete occlusion in MI.

What causes Q waves on ECG?

Permanent myocardial necrosis leading to loss of electrical activity in infarcted tissue.

How do plaque vulnerability factors increase rupture risk?

Large lipid core, thin fibrous cap, inflammation, and few smooth muscle cells increase vulnerability.

Why serial ECGs are important in ACS?

ECG changes evolve; serial tracings detect dynamic ST/T changes and guide treatment.

Nursing role post-ACS relevant to education.

Teach meds, activity progression, risk-factor modification (smoking, lipids, BP), and signs of recurrence.

Differentiate HFrEF vs HFpEF in one line.

HFrEF (systolic) = reduced EF due to decreased contractility; HFpEF (diastolic) = preserved EF with impaired filling/stiff ventricle.

Typical EF ranges for HFrEF and normal EF.

HFrEF: EF <40%; Normal EF: 55-70%.

Mechanism of pulmonary edema in left-sided HF.

Elevated left atrial pressure increases pulmonary capillary hydrostatic pressure fluid into alveoli.

Right-sided HF common signs.

Peripheral edema, JVD, hepatosplenomegaly, abdominal discomfort, nocturia.

Frank-Starling compensation effect in heart failure.

Increased preload stretches fibers improving SV short-term, but chronic overload worsens failure.

How does RAAS worsen heart failure?

Decreased CO activates RAAS angiotensin II causes vasoconstriction and aldosterone-mediated fluid retention, increasing preload/afterload.

Role of natriuretic peptides.

ANP/BNP promote natriuresis and vasodilation; BNP rises in HF and helps diagnosis/monitoring.

Why chronic SNS activation is harmful in HF?

Sustained catecholamines increase HR, arrhythmia risk, and myocardial oxygen demand causing remodeling.

S3 vs S4 heart sounds indicate which pathology?

S3: systolic dysfunction/volume overload (HFrEF); S4: stiff ventricle/diastolic dysfunction (HFpEF).

Primary cause of right-sided HF.

Most commonly secondary to left-sided HF; also pulmonary disease (cor pulmonale).

First-line objective in acute decompensated HF care.

Reduce preload and afterload (diuretics, vasodilators), oxygenation, and treat underlying triggers.

Why loop diuretics are used in HF?

They rapidly reduce preload by promoting diuresis, relieving pulmonary and peripheral congestion.

Complication risk in HF: arrhythmias and sudden death-why?

Structural remodeling and ischemia predispose to electrical instability and ventricular arrhythmias.

Clinical sign of volume overload to monitor daily.

Weight gain (1 L fluid ≈ 1 kg) and peripheral edema tracking.

Purpose of ACE inhibitors/ARBs in HF.

Reduce afterload, inhibit RAAS remodeling effects, improve survival in HFrEF.

How does pulmonary HTN lead to right HF?

Elevated pulmonary vascular resistance causes RV hypertrophy and eventual failure.

Nursing education point on medications in HF.

Emphasize adherence, monitor BP/HR, weight/daily weights, and report worsening symptoms promptly.

Difference between left-to-right and right-to-left shunts.

Left-to-right: oxygenated blood recirculates to lungs (acyanotic). Right-to-left: deoxygenated blood enters systemic circulation causing cyanosis.

PDA murmur classic description.

Continuous 'machinery' murmur loudest at left sternal border, heard in both systole and diastole.

ASD characteristic auscultatory finding.

Fixed splitting of S2 due to prolonged pulmonary valve closure.

Most common congenital heart defect.

Ventricular septal defect (VSD).

Eisenmenger syndrome pathophysiology in VSD.

Long-standing left-to-right shunt causes pulmonary vascular resistance increase shunt reversal to right-to-left and cyanosis.

Why PDA closure is important in neonates?

Persistent PDA causes pulmonary overcirculation, CHF, and risk of pulmonary vascular disease; closure reverses abnormal hemodynamics.

Primary problem in neonatal RDS.

Surfactant deficiency alveolar collapse, decreased compliance, hypoxemia.

Croup key features and emergency sign.

Barking cough and inspiratory stridor; severe airway obstruction (stridor at rest, retractions) is emergency.

Epiglottitis red flag.

Drooling, high fever, tripod position-do not examine throat with tongue depressor.

RSV bronchiolitis main pathophysiology.

Viral inflammation of bronchioles mucus plugs, air trapping, hypoxemia in infants.

Bronchiolitis typical infant symptoms.

Wheezing, tachypnea, poor feeding and apnea in very young infants.

When is bronchiolitis apnea a concern?

In very young or premature infants-requires immediate evaluation and monitoring.

Pediatric airway differences increasing obstruction risk.

Smaller airways and more compliant chest wall mean small edema causes big obstruction.

Prevention tip for RSV.

Hand hygiene and palivizumab prophylaxis for high-risk infants (per guidelines).

Define hypoxemia by PaO2 value.

PaO2 <60 mmHg indicates hypoxemia.