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
2
Q
What happens in acute arterial occlusion?
A
Sudden blockage of flow through a peripheral artery
3
Q
How does acute arterial occlusion happen?
A
Embolus or thrombus
Trauma
4
Q
How does acute arterial occlusion manifest? (6 p’s)
A
Pain, pallor, pulselessness, paralysis, paresthesia, polar
5
Q
What happens in chronic atherosclerotic occlusive disease?
A
Gradual decrease in blood flow (50% narrowing before onset of symptoms)
6
Q
How does chronic atherosclerotic occlusive disease happen?
A
Atherosclerosis
7
Q
How does chronic atherosclerotic occlusive disease manifest?
A
Claudication, weak pulses, cool, atrophy
8
Q
What is chronic venous insufficiency?
A
Failure of unidirectional flow through venous system often due to fault valves in veins
9
Q
What are manifestation of chronic venous insufficiency
A
Tissue congestion, edema, reddened extremities, stasis dermatitis, impaired tissue nutrition -> venous stasis ulcers
10
Q
What is varicose veins?
A
Dilates blood vessels in lower extremities that develops when blood flow through veins is occluded
11
Q
How does varicose veins occur?
A
Congenital abnormality, DVT, prolonged pressure on abdominal veins, prolonged standing -> increased venous pressure and vascular stretching
12
Q
What is DVT?
A
Deep vein thrombosis/thrombophlebitis
Presence of thrombus and inflammatory process in vessel, usually occurring in lower extremities
13
Q
What are the 3 factors associated with DVT development?
A
Virchow’s triad:
Venous stasis
Hypercoagulable state
Vascular injury
14
Q
How does DVT manifest?
A
Initially asymptomatic
Pain, swelling, muscle tenderness, fever, malaise
Can dislodge and travel
15
Q
What is vasculitis?
A
Inflammatory disorders affect vessel wall
16
Q
How does vasculitis manifest?
A
Fever, myalgia, malaise
17
Q
What causes vasculitis?
A
Vascular injury
Infectious agents
Autoimmune disorders
Secondarily
18
Q
What is vasculitis in smaller vessels called?
A
Wegener granulomatosis
19
Q
What is vasculitis in medium vessels called?
A
Polyarteritis nodosa, Kawasaki disease
20
Q
What is vasculitis in larger vessels called?
A
Giant cell (temporal) arteritis - Can obstruct blood flow to eye and lead to blindness
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
22
Q
What are risk factors for hypertensive vascular disease?
A
Genetic predisposition Age Race Insuline resistance High salt intake Obesity Excessive alcohol consumption
23
Q
What is essential HTN?
A
Elevated BP not due to another condition
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
25
What can uncontrolled HTN lead to?
```
LV hypertrophy
Heart failure
Atherosclerosis
Kidney disease
Retinopathy
Stroke
```
26
What is the renin-angiotensinogen-aldosterone system?
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
27
What is secondary HTN?
HTN due to another disease process
28
What are some causes of secondary HTN?
Renal HTN
Adrenocortical hormone dysfunction
Pheochromocytoma
Oral contraceptives
29
How does renal HTN occur?
Glomerulonephritis, acute/chronic renal failure, UTI, polycystic kidney disease
30
What happens in renal HTN?
Dysfunction of renin-angiotensin-aldosterone system
| Decreased flow through kidney -> renin production
31
How does Adrenocortical hormone dysfunction occur?
Increase aldosterone due to adrenal hyperplasia or excessive release of glucocorticoids due to Cushing's disease
Na+/H2O water retention
32
How does Pheochromocytoma occur?
Excessive release of catecholamines from tumor in adrenal medulla
33
How do oral contraceptives cause secondary HTN?
Estrogens and synthetic progesterones cause Na retention
34
How does Cushing's disease cause secondary HTN?
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
35
What is a hiatal hernia?
Protrusion of stomach through esophageal hiatus in the diaphragm caused by pressure and weak esophageal hiatus
36
What are the two types of hiatal hernias?
Sliding
| Paraesophageal hernia
37
What are the two types of sliding hernias?
```
Small hernia (95%)
Large sliding hernia
```
38
What is a large sliding hernia associated with?
Severe esophagitis, which can lead to Barrett esophagus from metaplastic changes
39
What happens with paraesophageal hernias?
Portion of the stomach rises alongside the esophagus
Can protrude into thoracic cavity
Can become strangled
40
What is GERD?
Gastroesophageal reflux disease - backwards movement of stomach contents up the esophagus
41
What is the most common GI condition?
GERD
42
What happens in GERD?
Lower esophageal sphincter is relaxed and reflux occurs
43
What will exacerbate GERD?
Anything increasing pressure in the abdomen
44
What causes GERD?
```
Weak LES
Irritating reflux material (pH <4)
Decreased clearance of refluxed material
Delayed gastric emptying -> pressure on LES
Decreased salivation
```
45
What are the two types of esophageal cancer?
Squamous
| Adenocarcinoma
46
What causes squamous esophageal cancer?
Alcohol/tobacco use
| 90% of esophageal cancer
47
What is adenocarcinoma esophageal cancer?
Barrett's esophagus/metaplastic changes -> dysplasia
48
What are symptoms of esophageal cancer?
Dysphagia
Weight loss
Pain on swallowing
49
What are Mallory-Weiss tears?
Longitudinal tears in the esophagus that often occur at the gastro-esophageal junction
50
What are Mallory-Weiss tears associated with?
Chronic alcoholism and uncontrolled vomiting
51
What can Mallory-Weiss tears cause?
Upper-GI bleeds because tears can become deep and affect blood vessels
52
What is the pathogenesis of Mallory-Weiss tears?
Impaired relaxation of LES between bouts of vomiting -> stretching and tearing
53
What can happen with Mallory-Weiss tears?
Can penetrate the walls of the esophagus and potentially cause mediastinitis
54
What are treatments for Mallory-Weiss tears?
```
Vasoconstrictive medications
Balloon compression (Sengstaken-Blakemore tube) to compress on bleeding sections
```
55
What are some gastric protective mechanisms?
Impermeable epithelial cell covering
Selective transport of H+ and HCO3-
Characteristics of gastric mucous
Actions of prostaglandins
56
What are characteristics of impermeable epithelial cell coverings?
Tightly bound
| Covered with lipid layer that prevents diffusion of ionized water-soluble molecules
57
What are characteristics of transport of H+ and HCO3-?
Balance is equal unless there is damage
| Reduction in blood flow -> lower HCO3-
58
How do prostaglandins affect H+ and HCO3-?
No prostaglandins -> removal of protective mechanism -> more H+ produced and less bicarb produced -> more acidic environment in stomach
59
What are characteristics of gastric mucous?
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
What are actions of prostaglandins?
Decrease acid secretion
Increase HCO3- secretion
Increase blood flow
ASA and NSAIDS reduce production of prostaglandins
61
What is gastritis?
Inflammation of gastric mucousa
62
What is acute gastritis?
Transient inflammation accompanied by hemorrhage into mucosa
63
What could acute gastritis result in?
Sloughing of mucosa
64
What is acute gastritis more commonly associated with?
Local irritants
65
What can cause acute gastritis?
Serious physiological stress
66
What is chronic gastritis?
Chronic inflammation leading to reduction of glandular epithelium
67
Does chronic gastritis include visible erosions?
No
68
What is the most common cause of chronic gastritis?
Helicobacter pylori
69
How does Helicobacter pylori cause chronic gastritis?
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
What can chronic gastritis lead to?
Gastric cancer and peptic ulcers
71
What are the most common types of peptic ulcers?
Duodenal and gastric ulcers
72
What are risk factors for peptic ulcer disease?
H. pylori
| Use of ASA and NSAIDs
73
How do H. pyloria, ASA, and NSAIDs cause peptic ulcer disease?
Interfere with protective effects of gastric mucosa
Inhibit prostaglandin synthesis
Induce inflammation and production of cytokines
74
What is pain from peptic ulcer disease associated with?
Empty stomach because nothing buffers the acid
| Pain -> food -> relief
75
When do gastric ulcers cause pain?
1-2 hours after eating
76
When do duodenal ulcers cause pain?
2-5 hours after a meal
77
What causes stress ulcers?
Physiologic stress
78
What factors precipitate stress ulcers?
Ischemia due to shunting of blood away from stomach (decrease clearance of H+)
Bile salts entering stomach (due to poor motility, increase acidity)
79
What is IBS?
Variable chronic and acute symptoms not attributable to structural or biochemical abnormalities
80
What causes IBS?
Unsure, but it may be due to dysregulation of intestinal sensory and/or motor function
81
What are symptoms of IBS?
Pain/cramping, altered function, flatulence, bloating, nausea
82
What are hall mark symptoms of IBS?
Associated with stress
No symptoms at night
Relief with defecation
Change in bowel habits
83
What are the two disorders of IBD?
Crohn's disease
| Ulcerative colitis
84
What is Crohn's disease?
Development of granulomatous lesions
85
What is ulcerative colitis?
Inflammation leading to ulceration
86
What happens in IBD?
The immune system may attack normal flora - autoimmune disorder
87
What causes IBD?
Possible genetic susceptibility
| Environmental triggers start the process
88
What are characteristics of Crohn's disease?
```
Submucosal
Can affect entire GI tract
Skip lesions
Bleeding rare
Fistulas/strictures common
```
89
What are characteristics of Ulcerative colitis?
```
Mucosal
Restricted to colon and rectum
Continuous
Bleeding is common
Fistulas/strictures are rare
```
90
What are skip lesions?
Development of granulomas with normal areas in between
91
What is a stricture?
Basically a stenosis - granulomas develop and impede travel through colon
92
What is diverticulosis?
When the mucosal layer herniates through the muscular layer
| Develop outpouching from buildup of pressure inside colon (from chronic constipation)
93
Where does diverticulosis usually occur?
Sigmoid colon
94
Does diverticulosis affect African nations/underdeveloped countries?
Essentially non-existent there
95
What is diverticulitis?
Inflammation/infection of diverticuli
96
What is appendicitis?
Enflamed, swollen, gangrenous appendix
97
What causes appendicitis?
Intraluminal obstruction with fecalith (poop stone) or twisting
98
What is appendicitis associated with?
Stretching due to inflammation
99
What is celiac disease?
Immune-mediated disorder initiated by gluten-containing products
100
What causes celiac disease?
Inappropriate T cell mediated immune response against gluten protein
101
What does the immune response in celiac disease result in?
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
What are intestinal polyps?
A mass that protrudes into the lumen of the intestine (most commonly large intestine)
103
What are adenomatous polyps?
Benign neoplasms of glandular-type tissue that arise from mucosa to replace cells being shed
104
How do adenomatous polyps form?
Excessive proliferation
| Decreased apoptosis and retaining the ability to replicate
105
What is a tubular intestinal polyp?
Smooth sphere attached to mucosa by a stalk
| 65% of benign adenomas
106
What is a villous intestinal polyp?
Broad based polyp with a cauliflower like surface
| 10%
107
What type of intestinal polyp is more likely to contain malignant cells?
Villous
108
What is a tubulovillous intestinal polyp?
Polyp that contains both types of growths
109
What factors increase the risk of colorectal cancer?
```
History of IBD or polyps
Familial adenomatous polyposis (mutation of chromosome 5)
Increased fat intake
Refined sugars
Lack of ACE vitamins
```
110
How is fiber related to colorectal cancer?
Increases bulk and removes potential carcinogens
111
What does colon cancer typical begin as?
Adenomatous polyps
| Dysplastic changes vary
112
How is ASA (aspirin) related to colorectal cancer?
Protective against it, possible from production of prostaglandins
113
What is hepatitis?
Inflammation of the liver
114
What causes hepatitis?
Viruses
Autoimmune disease
Reaction to toxins
Secondary to other disease
115
What are 2 mechanisms of injury for viral hepatitis?
Direct cellular injury
| Immune response against antigens
116
How does immune response play a role in viral hepatitis?
Strong immune response -> elimination of virus, but cellular injury
Weak immune response -> incomplete elimination of virus and less cellular injury
117
What are the 3 stages of acute vital hepatitis?
```
Prodromal/preicteric phase
- General malaise, myalgia, arthralgia, anorexia
Icteric phase
- Jaundice, pruritis, liver tenderness
Convalescent phase
- Return to normal state
```
118
What are characteristics of Hep A?
Self-limiting
Fecal-oral transmission
Vaccine available
119
What are characteristics of Hep B?
Blood and body fluid transmission
IV drugs/multiple sex partners
Vaccine available
120
What are characteristics of Hep C?
IV drugs, multiple sexual partners
No vaccine
Most common cause of chronic hepatitis, cirrhosis, and hepatocellular cancer
121
What are characteristics of Hep D?
Requires Hep B
| Can convert mild Hep B to fulminant hepatitis
122
What are characteristics of Hep E?
Fecal-oral route
Similar to Hep A
High mortality among pregnant women
Common in India, Southeast Asia, Africa, Mexico
123
How do antibodies react to Hep A exposure?
IgM arrive first then fade away
IgG take over and slowly rise
- More effective at eliminating virus
124
How do antibodies react to Hep B exposure?
IgM comes and then leaves
| IgG comes and remains as antibodies
125
What causes alcoholic liver disease?
Acetaldehyde has toxic effects on liver cells and function
| Free radicals damaging cells
126
What are effects of acetaldehyde?
Impede production of ATP
Prevents detoxification of free radicals
Promotes collagen synthesis
127
What are the 3 stages of alcoholic liver disease?
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
What happens in cirrhosis?
Viral hepatitis
Toxicity
Biliary obstruction
Non-alcoholic fatty liver disease (abnormal uptake and metabolism of lipids often due to insulin resistance)
129
What is liver failure?
Loss of 80-90% of liver function
130
What does liver failure impair?
Synthesis by substances of liver
- Albumin, coagulation factors, cholesterol, bile salts
Metabolism of chemicals
- Ammonia, drugs, toxins, bilirubin
131
What can liver failure cause?
Edema in legs
Higher risk of clotting
Hepatic encephalopathy (mental status change from raised ammonia)
132
What is cholelithiasis?
Gallstones
| - Precipitation of cholesterol, bilirubin, and other substances
133
What causes cholelithiasis?
Composition of bile/excessive secretion of cholesterol into bile
Stasis of bile
Inflammation of gallbladder
134
What is Cholecystitis?
Inflammation of gallbladder
Obstruction causes release of enzymes into gallbladder
85-90% associated with gallstones
135
What happens in Cholecystitis?
Obstruction causes release of enzymes into gallbladder
| Disruption of gallbladder lining
136
What is acute pancreatitis?
Inflammatory process of pancreas
137
What causes pancreatitis?
Autodigestion of pancreas by inappropriately activated pancreatic enzymes
Gallstones and alcohol abuse
138
What can pancreatitis cause?
SIRS
139
What steps occur in pancreatitis?
Activation of trypsin -> many digestive enzymes cause injury -> inflammatory response
SIRS and multi-organ failure can follow
