Test 2

What is the first-line treatment for hypertensive urgency?

Oral medications over 24-48 hours.

What is the primary cause of essential hypertension?

There is no single identifiable cause; it is driven by genetic predisposition, advanced age, high sodium intake, obesity, stress, and smoking.

What percentage of hypertension cases are classified as secondary hypertension?

5-10%

Name one condition that can cause secondary hypertension.

Renal artery stenosis, chronic kidney disease (CKD), pheochromocytoma, or primary aldosteronism.

What is the role of renin in the RAAS system?

Renin is released by the juxtaglomerular cells of the kidneys and converts Angiotensinogen into Angiotensin I.

What does ACE stand for and what is its function?

Angiotensin-Converting Enzyme; it converts Angiotensin I into Angiotensin II.

What effect does Angiotensin II have on blood pressure?

It causes powerful systemic vasoconstriction and stimulates the adrenal cortex to release Aldosterone, increasing blood volume.

What are the blood pressure readings for Stage 1 Hypertension?

Systolic 130-139 mmHg or Diastolic 80-89 mmHg.

What is the definition of a hypertensive crisis?

Blood pressure greater than 180/120 mmHg with acute target organ damage.

What are common side effects of ACE inhibitors?

Dry cough, hyperkalemia, and angioedema.

How do ARBs differ from ACE inhibitors?

ARBs block Angiotensin II receptors directly and do not cause the dry cough associated with ACE inhibitors.

What is the mechanism of action of beta-blockers?

They block β1 receptors in the heart, decreasing heart rate and cardiac output.

What is a common side effect of calcium channel blockers?

Peripheral edema, constipation, and bradycardia (with non-dihydropyridines).

What is the expected laboratory finding in metabolic acidosis?

Low pH and low HCO3-.

What are the early signs of hypovolemic shock?

Mild tachycardia, tachypnea, cool/pale skin, and delayed capillary refill.

What happens during late-stage hypovolemic shock?

Compensatory mechanisms fail, leading to tissue hypoxia, anaerobic metabolism, and metabolic acidosis.

What is the primary intervention for fluid resuscitation in dehydration?

Isotonic crystalloids (0.9% Normal Saline or Lactated Ringer's).

What is the definition of myocardial infarction?

Ischemia leading to myocardial tissue necrosis, typically from coronary artery occlusion.

What does the Left Anterior Descending artery supply?

The anterior wall of the left ventricle.

What are common symptoms of a myocardial infarction?

Crushing chest pain, diaphoresis, nausea, vomiting, and dyspnea.

What are the most specific cardiac biomarkers for myocardial injury?

Troponin I and T.

What is the MONA protocol for emergency chest pain management?

Morphine, Oxygen, Nitroglycerin, and Aspirin.

What is the effect of nitroglycerin in myocardial infarction?

It is a potent vasodilator that reduces myocardial oxygen demand.

What is the significance of elevated lactic acid in shock?

It indicates anaerobic metabolism due to inadequate tissue perfusion.

What is the expected change in hemoglobin and hematocrit during acute hemorrhage?

Decreased in acute hemorrhage due to fluid shifts.

What positioning is recommended for a patient in hypovolemic shock?

Modified Trendelenburg (legs elevated 45 degrees) to promote venous return.

What is the primary use of nitroglycerin?

It is a potent vasodilator that reduces myocardial oxygen demand.

What should be checked before administering nitroglycerin?

Blood pressure; hold if systolic is less than 90 mmHg.

What is the recommended dosage of aspirin for preventing platelet aggregation?

162-325 mg chewed immediately.

What is the purpose of heparin infusions in anticoagulant therapy?

To prevent further clot formation before/during Percutaneous Coronary Intervention (PCI).

What are the signs of bleeding to monitor for during heparin therapy?

Bleeding gums, hematuria, dark tarry stools.

What triggers Disseminated Intravascular Coagulation (DIC)?

Massive systemic inflammation such as sepsis, trauma, or abruptio placentae.

What is the first phase of DIC pathophysiology?

Trigger Phase: Massive endothelial damage and release of Tissue Factor.

What occurs during the clotting phase of DIC?

Microthrombi formation, leading to occlusion of small vessels.

What happens in the consumption phase of DIC?

Depletion of platelets, fibrinogen, and clotting factors occurs.

What characterizes the hemorrhage phase of DIC?

Profuse systemic bleeding from various orifices due to depleted clotting factors.

What laboratory findings are associated with DIC?

Markedly decreased platelets and fibrinogen, prolonged PT and aPTT, and significantly elevated D-Dimer.

What is the primary treatment for DIC?

Treat the underlying cause, such as eradicating sepsis or delivering the placenta.

What is cirrhosis?

End-stage, irreversible scarring of hepatic tissue, usually from chronic alcohol abuse or hepatitis.

What are the signs of portal hypertension due to cirrhosis?

Splenomegaly and esophageal varices.

What causes jaundice in cirrhosis?

The liver's inability to conjugate or excrete bilirubin.

What is hepatic encephalopathy?

A condition where the damaged liver cannot convert neurotoxic ammonia into urea, leading to confusion and lethargy.

What are the expected lab findings in cirrhosis?

Elevated liver enzymes, elevated ammonia, decreased albumin, and prolonged PT/INR.

What is the role of lactulose in treating hepatic encephalopathy?

It acidifies the gut, converting ammonia into ammonium, which is excreted in stool.

What is the purpose of administering spironolactone in ascites management?

It blocks RAAS fluid retention to reduce fluid accumulation.

What is hypoparathyroidism?

A deficiency of Parathyroid Hormone (PTH), often due to surgical removal or damage to parathyroid glands.

What are the signs of hypocalcemia?

Numbness, tingling, muscle cramps, tetany, and laryngospasm.

What is a positive Trousseau's sign?

Carpal spasm induced by inflating a BP cuff above systolic pressure for 3 minutes.

What is the effect of low calcium on nerve and muscle excitability?

It lowers the threshold for depolarization, leading to neuromuscular irritability.

What is the acute management for severe hypocalcemia?

Administer IV Calcium Gluconate slowly.

What are the chronic management strategies for hypoparathyroidism?

High-dietary calcium, oral calcium carbonate supplements, and Calcitriol.

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