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Pathophysiology > Pathophysiology Oral Topics > Flashcards

Pathophysiology Oral Topics Flashcards

1
Q

Cellular Phase of Acute Inflammation

A

It involes the delivery of leukocytes, mainly neutrophil, to the site of injury so they can use their host defence function. This phase is devided into margination, adhesion, transmigration, chemotaxis and phagocytosis.

First the leukocyte will marginate to the vessel surface. Then it will adhere to the surface and transmigrate from the vascular space to the extravascular space which is facilitated by complementary adhesion molecules such as selectins and integrins. After the extravasation, the neutrophil will undergo chemotaxis which is a process of guiding the transmigrated leukocytes to the site of cell injury.

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2
Q

Pathophysiology of Cardiac Insufficiency

A
  • Definition of Heart Failure
  • Causes of Heart Failure
  • Forms of Heart Failure
  • Symptoms of Heart Failure
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3
Q

Pathophysiological compensatory mechanisms in heart failure

A
  • Increases in left ventricular volume and pressure
  • Ventricular remodeling
  • Neurohormonal activation
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4
Q

What are the different type of hyperlipidemias in Fredrickson/WHO classification called?

A

Type I - Familial lipoprotein lipase deficiency
Type IIA - Familial hypercholesterolemia
Type IIB - Familial hyperbetalipoproteinemia
Type III - Familial dysbetalipoproteinemia
Type IV - Familial combined hyperlipidemia
Type V - Mixed hyperlipoproteinemia

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5
Q

Myocardial stunning

A

Refers to a prolonged period (hours, days) of reversible myocardial dysfunction after an ishemic event.

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6
Q

Hibernation

A

Occurs in the setting of chronic ischemia when oxygen delivery is adequate to maintain myocardial viability but inadequate to maintain normal function. The clinical importance of the hibernating states is that restoration of blood flow to the involved myocardium results in improved mechanical function

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7
Q

Regional myocardial hypoxia causes

A

Anaerobic glycolysis, lactate production, intracellular acidosis, and disordered calcium homeostasis. These intracellular changes induce abnormalities in myocardial relaxation, leading to reduced compliance and contraction, which cause regional wall abnormalities. Finally, ECG evidence of ischemia occurs, and angina pectoris ensues.

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8
Q

The size and pattern of an infarct depends on

A
  • Location and extent of occlusion
  • Amount of heart tisse supplied by the vessel
  • Duration of the occlusion
  • Metabolic needs of the affected tissue
  • Extent of collateral circulation
  • Heart rate, blood pressure, and cardiac rhythm
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9
Q

Arrhytmias are generally produced by one of three mechanisms

A

Enhanced automaticity
Triggered activity
Reentry

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10
Q

Delayed afterdepolarizations (DADs)

A

The presence of increased Calcium in the sarcoplasmic reticulum and cytosol leads to induction of DADs

Digitalis toxicity, catecholamines and reperfusion ventricular tachycardia (ischemia) can lead to increased calcium –> Thus, the formation of DADs

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11
Q

Early afterdepolarizations (EADs)

A

Arise from action potential prolongation and reactivation of depolarizing currents.

Hypokalemia, Hypomagnesemia, Bradycardia and drugs can predispose to generation of EADs.

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12
Q

Arrhythmias from abnormal automaticity

A

Sinus bradycardia
Sinus tachycardia
Atrial tachycardia
Ventricular fibrillation

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13
Q

Arrhythmias from triggered automaticity

A

Due to EADs:
Polymorphic ventricular tachycardia
Atrial tachycardia
Torsades de pointes

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14
Q

Arrhythmias from reentry

A 
AVNRT
AVRT
Atrial fibrillation
Atrial flutter
Ventricular fibrillation
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15
Q

Most common complications of PUD

A

Hemorrhage
Perforation
Penetration
Gastric outlet obstruction

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16
Q

Four major causes of chronic diarrhea

A

Presence of hyperosmotic luminal contents
Increased intestinal secretory processes
Inflammatory conditions, and infectious processes
Factitious diarrhea

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17
Q

What is ulcerative proctitis, proctosigmoiditis, and pancolitis

A

It’s the length of lesion in ulcerative colitis. Ulcerative proctitis involve the rectum alone, proctosigmoiditis involves the rectum and sigmoid colon and pancolitis involves the entire colon.

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18
Q

Three factors that contribute to the formation of gallstones

A

Abnormalities in the composition of bile
Stasis of blie
Inflammation of the gallbladder

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19
Q

Causes of Ascites

A 
Cirrhosis
Portal hypertension
Right-sided heart failure
Nephrotic syndrome
Hypoalbuminemia
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20
Q

GERD complications

A

Strictures of the esophagus
Barret’s esophagus
Hemorrhage
Erosive esophagitis

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21
Q

Release of Kallikrein and Chymotrypsin results in

A

increased capillary membrane permeability, leading to the leakage of fluid into the interstitum and development of edema and relative hypovolemia.

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22
Q

Release of Elastase results in

A

leads to dissolution of the elastic fibers of the blood vessels and cuts, leading to hemorrhage.

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23
Q

Release of Phospholipase A results in

A

in the presence of bile, destroys phospholipids of cell membranes causing severe pancreatic and adipose tissue necrosis.

24
Q

Release of Lipase results in

A

flows into damaged tissue and is absorbed into systemic circulation, resulting in fat necrosis of the pancreas and surrounding tissue.

25
Q

Pulmonary complications of Pancreatitis

A

Atelectasis
Pleural effusion
ARDS

26
Q

Cardiovascular complications of Pancreatitis

A

Cardiogenic shock

27
Q

Neurological complications of Pancreatitis

A

Pancreatic encephalopathy

28
Q

Metabolic complications of Pancreatitis

A

Metabolic acidosis
Hypocalcemia
Hyperglycemia

29
Q

Hematologic complications of Pancreatitis

A

DIC

GI bleeding

30
Q

Renal complications of Pancreatitis

A

Prerenal failure

31
Q

Subacute Granulomatous (De Quervain) Thyroiditis is caused by

A

Viral infections

32
Q

Subacute Lymphocytic Thyroidits (Hashimotos) (Chronic) is caused by

A

Destruction of the normal thyroid architecture by lymphocytic infiltration result in hypothyroidism and goiter

33
Q

Manifestations of hypoparathyroidism

A

Tetany with muscle cramps
Paresthesias
Prolonged QT
Hypotension

34
Q

How can hyperparathyroidism lead to kidney stones

A

Because of elevation in ionized calcium, and increased urinary excretion of both calcium and phosphorus

35
Q

In hypopituitarism, which hormones are lost first

A

GH, LH and FSH followed by TSH, then ACTH, and finally prolaction

36
Q

Dopamine beta hydroxylase deficiency

A

is a condition involving inadequate dopamine beta-hydroxylase. It is characterized by increased amounts of serum dopamine and the absence of norepinephrine (NE) and epinephrine. Dopamine is released, as a false neurotransmitter, in place of norepinephrine

37
Q

Types of hormonal hypofunction

A

Hypothyroidism
Hypoparathyroidism
Addison’s disease

38
Q

Types of hormonal hyperfunction

A 
Hyperthyroidism
Hyperparathyroidism
Acromegaly
Prolactinoma
Conn's syndrome
Cushing syndrome
39
Q

Hormones associated with the stress response

A

Catecholamines (norepinephrine, epinephrine)
CRH –> ACTH –> Cortisol
Aldosterone
ADH

40
Q

Coordinated release of the neurohormones in stress results in

A
  • Mobilization of energy
  • A sharpened focus and awareness
  • Increased cerebral blood flow and glucose utilization
  • Enhanced cardiovascular and respiratory functioning
  • Redistribution of blood flow to the brain and muscles
  • Modulation of the immune response
  • Inhibition of reproductive function, and a decrease in appetite
41
Q

Hypoxia can result from

A
  • Inadequate amount of oxygen in the air
  • Respiratory disease
  • Ischemia
  • Anemia
  • Edema
  • Inability of the cells to use oxygen
42
Q

ARDS is a clinical syndrome characterised by

A

Acute onset of severe dyspnea
Hypoxemia
Pulmonary infiltrates

43
Q

Causes of hypoxemic respiratory failure

A
  • COPD
  • Restrictive lung disease
  • ARDS
44
Q

Cause of hypercapnic respiratory failure

A
  • Weakness or paralysis of respiratory muscles
  • Muscular dystrophy
  • Brain injury
45
Q

Primary causes of nephrotic syndrome

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis

46
Q

Secondary cause of nephrotic syndrome

A

Diabetes mellitus

SLE

47
Q

Minimal change disease is characterized by

A

Diffuse loss of podocytes or foot processes of the visceral epithelial cells of the glomeruli

48
Q

Membranous nephropathy is characterized by

A

Diffuse thickening of the glomerular basement membrane due to deposition of immune complexes

49
Q

Focal segmental glomerulosclerosis is characterized by

A

Sclerosis (increased collagen deposition) in some but not all glomeruli

50
Q

Acute renal failure is a syndrome characterized by

A

Abrupt decrease in GFR, increased BUN, disturbed regulation of ECF volume, acid base homeostasis and impaired drug excretion

51
Q

Intrinsic kidney injury can be divided into

A

Vasculature
Glomerulus
Tubules
Interstitium

52
Q

Complications of Acute kidney injury

A 
Hyperkalemia
Metabolic acidosis
Hypocalcemia
Hyperphosphatemia
Anemia
53
Q

Metabolic syndrome is characterized by

A
  • Hyperglycemia
  • Intra-abdominal obesity
  • High triglycerides, low HDL
  • Hypertension
  • Systemic inflammation
  • Abnormal fibrinogen
  • Abnormal function of vascular endothelium
  • Macrovascular disease (CHD, cerebrovascular and peripheral artery disease)
54
Q

Acute complications of Diabetes Mellitus

A

Hypoglycemia
Lactic acidosis
Diabetic ketoacidosis

55
Q

Chronic complications of Diabetes Mellitus

A 
Microvascular 
-Nephropathy
-Retinopathy
-Neuropathy
Diabetic foot
Macrovascular

Pathophysiology (20 decks)

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