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Pathophysiology exam 2 > Peripheral vascular disorders and the GI system > Flashcards

Peripheral vascular disorders and the GI system Flashcards

1
Q

What are the 2 types of peripheral arterial disease?

A

Acute arterial occlusion

Chronic atherosclerotic occlusive disease

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2
Q

What happens in acute arterial occlusion?

A

Sudden blockage of flow through a peripheral artery

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3
Q

How does acute arterial occlusion happen?

A

Embolus or thrombus

Trauma

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4
Q

How does acute arterial occlusion manifest? (6 p’s)

A

Pain, pallor, pulselessness, paralysis, paresthesia, polar

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5
Q

What happens in chronic atherosclerotic occlusive disease?

A

Gradual decrease in blood flow (50% narrowing before onset of symptoms)

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6
Q

How does chronic atherosclerotic occlusive disease happen?

A

Atherosclerosis

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7
Q

How does chronic atherosclerotic occlusive disease manifest?

A

Claudication, weak pulses, cool, atrophy

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8
Q

What is chronic venous insufficiency?

A

Failure of unidirectional flow through venous system often due to fault valves in veins

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9
Q

What are manifestation of chronic venous insufficiency

A

Tissue congestion, edema, reddened extremities, stasis dermatitis, impaired tissue nutrition -> venous stasis ulcers

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10
Q

What is varicose veins?

A

Dilates blood vessels in lower extremities that develops when blood flow through veins is occluded

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11
Q

How does varicose veins occur?

A

Congenital abnormality, DVT, prolonged pressure on abdominal veins, prolonged standing -> increased venous pressure and vascular stretching

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12
Q

What is DVT?

A

Deep vein thrombosis/thrombophlebitis

Presence of thrombus and inflammatory process in vessel, usually occurring in lower extremities

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13
Q

What are the 3 factors associated with DVT development?

A

Virchow’s triad:
Venous stasis
Hypercoagulable state
Vascular injury

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14
Q

How does DVT manifest?

A

Initially asymptomatic
Pain, swelling, muscle tenderness, fever, malaise
Can dislodge and travel

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15
Q

What is vasculitis?

A

Inflammatory disorders affect vessel wall

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16
Q

How does vasculitis manifest?

A

Fever, myalgia, malaise

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17
Q

What causes vasculitis?

A

Vascular injury
Infectious agents
Autoimmune disorders
Secondarily

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18
Q

What is vasculitis in smaller vessels called?

A

Wegener granulomatosis

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19
Q

What is vasculitis in medium vessels called?

A

Polyarteritis nodosa, Kawasaki disease

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20
Q

What is vasculitis in larger vessels called?

A 
Giant cell (temporal) arteritis
- Can obstruct blood flow to eye and lead to blindness
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21
Q

What is hypertensive vascular disease?

A

SBP greater than or equal to 140 mmHg and DBP greater than or equal to 90 mmHg

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22
Q

What are risk factors for hypertensive vascular disease?

A 
Genetic predisposition
Age
Race
Insuline resistance
High salt intake
Obesity
Excessive alcohol consumption
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23
Q

What is essential HTN?

A

Elevated BP not due to another condition

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24
Q

What is essential HTN thought to involve?

A

Kidney’s ability to regulate Na and H2O
Sympathetic hyper-reactivity
Renin-angiotensin-aldosterone system dysfunction

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25
Q

What can uncontrolled HTN lead to?

A 
LV hypertrophy
Heart failure
Atherosclerosis
Kidney disease
Retinopathy
Stroke
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26
Q

What is the renin-angiotensinogen-aldosterone system?

A

Renin -> angiotensinogen -> angiotensin 1 -> slight vasoconstriction -> angiotensin from lungs converts angiotensin 1 -> angiotensin 2 -> aldosterone from adrenal cortex -> promotion of retention of Na/H2O and release of K -> more fluid in blood vessels

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27
Q

What is secondary HTN?

A

HTN due to another disease process

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28
Q

What are some causes of secondary HTN?

A

Renal HTN
Adrenocortical hormone dysfunction
Pheochromocytoma
Oral contraceptives

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29
Q

How does renal HTN occur?

A

Glomerulonephritis, acute/chronic renal failure, UTI, polycystic kidney disease

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30
Q

What happens in renal HTN?

A

Dysfunction of renin-angiotensin-aldosterone system

Decreased flow through kidney -> renin production

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31
Q

How does Adrenocortical hormone dysfunction occur?

A

Increase aldosterone due to adrenal hyperplasia or excessive release of glucocorticoids due to Cushing’s disease
Na+/H2O water retention

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32
Q

How does Pheochromocytoma occur?

A

Excessive release of catecholamines from tumor in adrenal medulla

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33
Q

How do oral contraceptives cause secondary HTN?

A

Estrogens and synthetic progesterones cause Na retention

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34
Q

How does Cushing’s disease cause secondary HTN?

A

Tumor in pituitary gland -> excessive release of ACTH -> aldosterone release -> Na/H2O retention -> higher BP
Tumor of adrenal gland -> aldosterone -> Na/H2O retention -> higher blood volume

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35
Q

What is a hiatal hernia?

A

Protrusion of stomach through esophageal hiatus in the diaphragm caused by pressure and weak esophageal hiatus

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36
Q

What are the two types of hiatal hernias?

A

Sliding

Paraesophageal hernia

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37
Q

What are the two types of sliding hernias?

A 
Small hernia (95%)
Large sliding hernia
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38
Q

What is a large sliding hernia associated with?

A

Severe esophagitis, which can lead to Barrett esophagus from metaplastic changes

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39
Q

What happens with paraesophageal hernias?

A

Portion of the stomach rises alongside the esophagus
Can protrude into thoracic cavity
Can become strangled

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40
Q

What is GERD?

A

Gastroesophageal reflux disease - backwards movement of stomach contents up the esophagus

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41
Q

What is the most common GI condition?

A

GERD

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42
Q

What happens in GERD?

A

Lower esophageal sphincter is relaxed and reflux occurs

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43
Q

What will exacerbate GERD?

A

Anything increasing pressure in the abdomen

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44
Q

What causes GERD?

A 
Weak LES
Irritating reflux material (pH <4)
Decreased clearance of refluxed material
Delayed gastric emptying -> pressure on LES
Decreased salivation
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45
Q

What are the two types of esophageal cancer?

A

Squamous

Adenocarcinoma

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46
Q

What causes squamous esophageal cancer?

A

Alcohol/tobacco use

90% of esophageal cancer

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47
Q

What is adenocarcinoma esophageal cancer?

A

Barrett’s esophagus/metaplastic changes -> dysplasia

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48
Q

What are symptoms of esophageal cancer?

A

Dysphagia
Weight loss
Pain on swallowing

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49
Q

What are Mallory-Weiss tears?

A

Longitudinal tears in the esophagus that often occur at the gastro-esophageal junction

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50
Q

What are Mallory-Weiss tears associated with?

A

Chronic alcoholism and uncontrolled vomiting

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51
Q

What can Mallory-Weiss tears cause?

A

Upper-GI bleeds because tears can become deep and affect blood vessels

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52
Q

What is the pathogenesis of Mallory-Weiss tears?

A

Impaired relaxation of LES between bouts of vomiting -> stretching and tearing

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53
Q

What can happen with Mallory-Weiss tears?

A

Can penetrate the walls of the esophagus and potentially cause mediastinitis

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54
Q

What are treatments for Mallory-Weiss tears?

A 
Vasoconstrictive medications
Balloon compression (Sengstaken-Blakemore tube) to compress on bleeding sections
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55
Q

What are some gastric protective mechanisms?

A

Impermeable epithelial cell covering
Selective transport of H+ and HCO3-
Characteristics of gastric mucous
Actions of prostaglandins

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56
Q

What are characteristics of impermeable epithelial cell coverings?

A

Tightly bound

Covered with lipid layer that prevents diffusion of ionized water-soluble molecules

57
Q

What are characteristics of transport of H+ and HCO3-?

A

Balance is equal unless there is damage

Reduction in blood flow -> lower HCO3-

58
Q

How do prostaglandins affect H+ and HCO3-?

A

No prostaglandins -> removal of protective mechanism -> more H+ produced and less bicarb produced -> more acidic environment in stomach

59
Q

What are characteristics of gastric mucous?

A

Water insoluble mucous gel adheres to gastric mucosa
- Protective against pepsin
- Traps HCO3-, creating alkaline barrier
Water soluble mucous mixes with stomach contents
- Lubricates and protects mucosa

60
Q

What are actions of prostaglandins?

A

Decrease acid secretion
Increase HCO3- secretion
Increase blood flow
ASA and NSAIDS reduce production of prostaglandins

61
Q

What is gastritis?

A

Inflammation of gastric mucousa

62
Q

What is acute gastritis?

A

Transient inflammation accompanied by hemorrhage into mucosa

63
Q

What could acute gastritis result in?

A

Sloughing of mucosa

64
Q

What is acute gastritis more commonly associated with?

A

Local irritants

65
Q

What can cause acute gastritis?

A

Serious physiological stress

66
Q

What is chronic gastritis?

A

Chronic inflammation leading to reduction of glandular epithelium

67
Q

Does chronic gastritis include visible erosions?

A

No

68
Q

What is the most common cause of chronic gastritis?

A

Helicobacter pylori

69
Q

How does Helicobacter pylori cause chronic gastritis?

A

Migrate through mucous layer with flagella
Secrete urease -> coverts urea to ammonia -> buffers stomach acid
Produces enzymes/toxins that interfere with protective mucosa
Inflammation occurs
Immune response stimulated -> proinflammatory cytokines -> neutrophils and lymphocytes recruited

70
Q

What can chronic gastritis lead to?

A

Gastric cancer and peptic ulcers

71
Q

What are the most common types of peptic ulcers?

A

Duodenal and gastric ulcers

72
Q

What are risk factors for peptic ulcer disease?

A

H. pylori

Use of ASA and NSAIDs

73
Q

How do H. pyloria, ASA, and NSAIDs cause peptic ulcer disease?

A

Interfere with protective effects of gastric mucosa
Inhibit prostaglandin synthesis
Induce inflammation and production of cytokines

74
Q

What is pain from peptic ulcer disease associated with?

A

Empty stomach because nothing buffers the acid

Pain -> food -> relief

75
Q

When do gastric ulcers cause pain?

A

1-2 hours after eating

76
Q

When do duodenal ulcers cause pain?

A

2-5 hours after a meal

77
Q

What causes stress ulcers?

A

Physiologic stress

78
Q

What factors precipitate stress ulcers?

A

Ischemia due to shunting of blood away from stomach (decrease clearance of H+)
Bile salts entering stomach (due to poor motility, increase acidity)

79
Q

What is IBS?

A

Variable chronic and acute symptoms not attributable to structural or biochemical abnormalities

80
Q

What causes IBS?

A

Unsure, but it may be due to dysregulation of intestinal sensory and/or motor function

81
Q

What are symptoms of IBS?

A

Pain/cramping, altered function, flatulence, bloating, nausea

82
Q

What are hall mark symptoms of IBS?

A

Associated with stress
No symptoms at night
Relief with defecation
Change in bowel habits

83
Q

What are the two disorders of IBD?

A

Crohn’s disease

Ulcerative colitis

84
Q

What is Crohn’s disease?

A

Development of granulomatous lesions

85
Q

What is ulcerative colitis?

A

Inflammation leading to ulceration

86
Q

What happens in IBD?

A

The immune system may attack normal flora - autoimmune disorder

87
Q

What causes IBD?

A

Possible genetic susceptibility

Environmental triggers start the process

88
Q

What are characteristics of Crohn’s disease?

A 
Submucosal
Can affect entire GI tract
Skip lesions
Bleeding rare
Fistulas/strictures common
89
Q

What are characteristics of Ulcerative colitis?

A 
Mucosal
Restricted to colon and rectum
Continuous
Bleeding is common
Fistulas/strictures are rare
90
Q

What are skip lesions?

A

Development of granulomas with normal areas in between

91
Q

What is a stricture?

A

Basically a stenosis - granulomas develop and impede travel through colon

92
Q

What is diverticulosis?

A

When the mucosal layer herniates through the muscular layer

Develop outpouching from buildup of pressure inside colon (from chronic constipation)

93
Q

Where does diverticulosis usually occur?

A

Sigmoid colon

94
Q

Does diverticulosis affect African nations/underdeveloped countries?

A

Essentially non-existent there

95
Q

What is diverticulitis?

A

Inflammation/infection of diverticuli

96
Q

What is appendicitis?

A

Enflamed, swollen, gangrenous appendix

97
Q

What causes appendicitis?

A

Intraluminal obstruction with fecalith (poop stone) or twisting

98
Q

What is appendicitis associated with?

A

Stretching due to inflammation

99
Q

What is celiac disease?

A

Immune-mediated disorder initiated by gluten-containing products

100
Q

What causes celiac disease?

A

Inappropriate T cell mediated immune response against gluten protein

101
Q

What does the immune response in celiac disease result in?

A

Inflammation and destruction of intestinal villi (less surface area for absorption -> water remain -> diarrhea)
Impair absorption of proteins, CHO, fats, vitamins
Can lead to cancers

102
Q

What are intestinal polyps?

A

A mass that protrudes into the lumen of the intestine (most commonly large intestine)

103
Q

What are adenomatous polyps?

A

Benign neoplasms of glandular-type tissue that arise from mucosa to replace cells being shed

104
Q

How do adenomatous polyps form?

A

Excessive proliferation

Decreased apoptosis and retaining the ability to replicate

105
Q

What is a tubular intestinal polyp?

A

Smooth sphere attached to mucosa by a stalk

65% of benign adenomas

106
Q

What is a villous intestinal polyp?

A

Broad based polyp with a cauliflower like surface

10%

107
Q

What type of intestinal polyp is more likely to contain malignant cells?

A

Villous

108
Q

What is a tubulovillous intestinal polyp?

A

Polyp that contains both types of growths

109
Q

What factors increase the risk of colorectal cancer?

A 
History of IBD or polyps
Familial adenomatous polyposis (mutation of chromosome 5)
Increased fat intake
Refined sugars
Lack of ACE vitamins
110
Q

How is fiber related to colorectal cancer?

A

Increases bulk and removes potential carcinogens

111
Q

What does colon cancer typical begin as?

A

Adenomatous polyps

Dysplastic changes vary

112
Q

How is ASA (aspirin) related to colorectal cancer?

A

Protective against it, possible from production of prostaglandins

113
Q

What is hepatitis?

A

Inflammation of the liver

114
Q

What causes hepatitis?

A

Viruses
Autoimmune disease
Reaction to toxins
Secondary to other disease

115
Q

What are 2 mechanisms of injury for viral hepatitis?

A

Direct cellular injury

Immune response against antigens

116
Q

How does immune response play a role in viral hepatitis?

A

Strong immune response -> elimination of virus, but cellular injury
Weak immune response -> incomplete elimination of virus and less cellular injury

117
Q

What are the 3 stages of acute vital hepatitis?

A 
Prodromal/preicteric phase
- General malaise, myalgia, arthralgia, anorexia
Icteric phase
- Jaundice, pruritis, liver tenderness
Convalescent phase
- Return to normal state
118
Q

What are characteristics of Hep A?

A

Self-limiting
Fecal-oral transmission
Vaccine available

119
Q

What are characteristics of Hep B?

A

Blood and body fluid transmission
IV drugs/multiple sex partners
Vaccine available

120
Q

What are characteristics of Hep C?

A

IV drugs, multiple sexual partners
No vaccine
Most common cause of chronic hepatitis, cirrhosis, and hepatocellular cancer

121
Q

What are characteristics of Hep D?

A

Requires Hep B

Can convert mild Hep B to fulminant hepatitis

122
Q

What are characteristics of Hep E?

A

Fecal-oral route
Similar to Hep A
High mortality among pregnant women
Common in India, Southeast Asia, Africa, Mexico

123
Q

How do antibodies react to Hep A exposure?

A

IgM arrive first then fade away
IgG take over and slowly rise
- More effective at eliminating virus

124
Q

How do antibodies react to Hep B exposure?

A

IgM comes and then leaves

IgG comes and remains as antibodies

125
Q

What causes alcoholic liver disease?

A

Acetaldehyde has toxic effects on liver cells and function

Free radicals damaging cells

126
Q

What are effects of acetaldehyde?

A

Impede production of ATP
Prevents detoxification of free radicals
Promotes collagen synthesis

127
Q

What are the 3 stages of alcoholic liver disease?

A

Fatty changes
- Accumulation of fat in hepatocytes (steatosis)
Alcoholic hepatitis
- Inflammation/necrosis of liver cells
- Hepatic tenderness, fever, nausea, anorexia, jaundice
- More common in binge drinkers
Cirrhosis
- Liver tissue replaced by fibrous tissue
- Onset of end-stage liver disease
- Portal HTN
- Portosystemic shunts (bypass route)

128
Q

What happens in cirrhosis?

A

Viral hepatitis
Toxicity
Biliary obstruction
Non-alcoholic fatty liver disease (abnormal uptake and metabolism of lipids often due to insulin resistance)

129
Q

What is liver failure?

A

Loss of 80-90% of liver function

130
Q

What does liver failure impair?

A

Synthesis by substances of liver
- Albumin, coagulation factors, cholesterol, bile salts
Metabolism of chemicals
- Ammonia, drugs, toxins, bilirubin

131
Q

What can liver failure cause?

A

Edema in legs
Higher risk of clotting
Hepatic encephalopathy (mental status change from raised ammonia)

132
Q

What is cholelithiasis?

A

Gallstones

- Precipitation of cholesterol, bilirubin, and other substances

133
Q

What causes cholelithiasis?

A

Composition of bile/excessive secretion of cholesterol into bile
Stasis of bile
Inflammation of gallbladder

134
Q

What is Cholecystitis?

A

Inflammation of gallbladder
Obstruction causes release of enzymes into gallbladder
85-90% associated with gallstones

135
Q

What happens in Cholecystitis?

A

Obstruction causes release of enzymes into gallbladder

Disruption of gallbladder lining

136
Q

What is acute pancreatitis?

A

Inflammatory process of pancreas

137
Q

What causes pancreatitis?

A

Autodigestion of pancreas by inappropriately activated pancreatic enzymes
Gallstones and alcohol abuse

138
Q

What can pancreatitis cause?

A

SIRS

139
Q

What steps occur in pancreatitis?

A

Activation of trypsin -> many digestive enzymes cause injury -> inflammatory response
SIRS and multi-organ failure can follow

Pathophysiology exam 2 (2 decks)

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