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Advanced Pathophysiology > GI > Flashcards

GI Flashcards

1
Q

What are the layers of the wall of the GI tract, starting with innermost:

A
  1. Mucosa
  2. Submucosa
  3. Muscularis
  4. Serosa

A networks of nerve is between each of the layers

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2
Q

What does the mucosal layer of the esophagus specialized function?

A

Stratified squamous epithelium that enables gliding of masticated food

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3
Q

What specialized function does the stomach mucosal layer have:

A

Thick glandular mucosa that provides mucus, acid, and proteolytic enzymes for digestion

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4
Q

What specialized function does the small intestine mucosal layer have:

A

Villious structure to provide large surface area for absorption

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5
Q

What specialized function does the large intestine mucosal layer have:

A

Lined with abundant mucus secreting cells that facilitate storage and evacuation of residue

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6
Q

What is the gut nervous system called and what does it innervate?

A

Enteric nervous system

Stomach muscle, secretory cells, endocrine cells, blood vessels

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7
Q

What is absorbed in the mouth?

A

Certain drugs that come in contact with the mucosa of the mouth are absorbed into the blood stream

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8
Q

What is absorbed in the stomach?

A

Water, simple sugars, alcohol

Water, alcohol, copper, iodide fluoride, molybdenum

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9
Q

What is absorbed in the small intestine?

A

The final steps of digestion; glucose, fructose, fatty acids, glycerol, amino acids are absorbed into the blood stream

Duodenum- Ca, Phos, Mag, Fe, vit A, D, E, K, etc
Jejunum- Lipids, monosaccharides, AA, small peptides, vit A, D, E, K, zinc, etc
Ileum- Bile salts/acids, vit C, vit B12, folate, vit D and K, Mag, etc

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10
Q

What is absorbed in the large intestine?

A

No chemical digestion, only by bacteria
Absorption of water, some minerals, and drugs

Water, vit K, biotin, Na, Cl, K, short chain fatty acid

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11
Q

What are the parts of the small intestine?

A

Duodenum to jejunum to ileum

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12
Q

A person unable to absorb bile salts may have had their __________ removed?

A

Ileum

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13
Q

What hormones stimulate gastric emptying?

A

Gastrin and motilin

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14
Q

What hormones delay gastric emptying?

A

Secretin and CCK

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15
Q

What are the 4 main general functions of the GI tract?

A
  1. Movement of nutrients-propulsion/mixing
  2. Secretion of digestive juices
  3. Digestion of nutrients
  4. Absorption of nutrients
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16
Q

What does salivary amylase in the mouth do?

A

Initiates carbohydrate digestion by breaking down polysaccharides into dextrin and maltose

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17
Q

What facilitates muscular movement through the esophagus?

A

Mucus
Muscle contractions
Gravity (not necessary)

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18
Q

Why is it important for the lower esophageal sphincter to remain tonically constricted?

A

To prevent the acidic gastric contents from moving into the esophagus. (GERD)

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19
Q

What is the muscular sphincter between the stomach and the duodenum and what does it do?

A

Pylorus/pyloric sphincter

Controls gastric emptying and limits reflux of bile from small intestine

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20
Q

Where are Chief cells located and what do they do?

A

Located in the stomach

They produce pepsinogen (the inactive form of pepsin)

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21
Q

Where are Parietal cells located and what do they do?

A

Located in the stomach

Produce HCl and intrinsic factor which is needed for vit B12 absorption

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22
Q

What do the mucous cells of the stomach do?

A

Produce an alkaline mucus that shields the stomach wall and neutralize acids close to wall

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23
Q

What is the longest portion of the GI tract?

A

Small intestine

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24
Q

Describe the lining of the small intestine:

A

The intestinal wall is marked by circular folds lines with intestinal villi to increase surface area for absorption and digestion. Each villi has microvilli which are covered by a brush border containing digestive enzymes

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25
Q

Where is the ileocecal valve and when does it open?

A

Located between the small and large intestine

Opened via peristaltic contractions

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26
Q

What are the 2 layers of the enteric nervous system and where are they located?

A
  1. Myenteric plexus; lies between the longitudinal and circular muscular layers (GI movement)
  2. Submucosal plexus; like in the submucosa (secretions and sensory functions)
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27
Q

What does gastrin do and where is it secreted?

A

Secreted in the stomach by G cells in response to food entry. It mediates gastric acid secretion and increases stomach motility. Promotes constriction of LES.

Also

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28
Q

What does CCK do and where is it secreted?

A

Secreted by I cells in the duodenum in response to fat. Stimulate release of pancreatic enzyme (lipase) and causes contraction of gallbladder and relaxation of sphincter of Oddi=bile released to duodenum.

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29
Q

What does secretin do and where is it secreted?

A

Secreted by the mucosa of the duodenum in response to acid from stomach. Stimulates pancreatic fluid and bicarb rich solution release = neutralize acidity in intestine

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30
Q

What do slow waves refer to?

A

Ongoing basic oscillation in membrane potential that occurs in the smooth muscle of the GI tract by myenteric nerve plexus (especially longitudinal muscle by)

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31
Q

The usual stimulus for peristalsis is ________

A

Distention of the intestinal walls

stimulates myenteric nerve plexus and circular constriction occurs to propel food forward

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32
Q

_________ contractions serve to keep the intestinal contents thoroughly mixed on a constant basis.

A

Segmental

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33
Q

What organs do the superior and inferior mesenteric plexus feed?

A

Superior- Pancreas, Small Intestine

Inferior- Large Intestine

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34
Q

All GI organs send deoxygenated blood to:

A

The liver via the portal vein

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35
Q

What organs does the splenic artery feed?

A

Stomach, Spleen, Pancreas

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36
Q

What is the major nerve of the parasympathetic nervous system that provides extensive innervation to the GI tract?

A

Vagus Nerve

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37
Q

What do the sympathetic nerve endings of the GI tract secrete and why is this important?

A

They secrete norepinephrine.
Promotes the inhibitory effect of the SNS on the GI tract and has ability to stop/block the movement of nutrients->Vomiting.

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38
Q

What provides chemical control in the Liver?

A

Insulin-like growth factor(somatomedin)
Angiotensinogen
Angiotensin
Thrombopoeitin

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39
Q

What provides chemical control in the Stomach?

A 
Gastrin
Ghrelin
Neuropeptide Y
Somatostatin
Histamine
Endothelin
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40
Q

What provides chemical control in the Duodenum?

A

Secretin

CCK

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41
Q

What provides chemical control in the Pancreas?

A

Insulin
Glucagon
Somatostatin
Pancreatic polypeptide

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42
Q

What provides chemical control in the Kidney?

A

Renin
EPO
Calcitriol
Thrombopoietin

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43
Q

How are starches digested?

A

(Mouth)
-Salivary amylase begins to break down the starch.
(Small Intestine)
-Pancreatic lipase
-Brush border enzymes (lactose, maltose, sucrose)
=simple sugars to be absorbed by capillaries and transported to the portal vein

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44
Q

How are proteins digested?

A

(Stomach)
-Pepsin in presence of HCl begins break down
(Small Intestine)
-Pancreatic enzymes (trypsin, chymotrypsin, carboxypeptidase)
-Brush border enzymes (aminopepsidases and dipepsidases)
=Amino acids to be absorbed by the capillaries and transported to the portal vein

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45
Q

How are unemulsified fats digested?

A

(Small Intestine)

  • Emulsifying agents (bile acids, fatty acids, monoglycerides, lecithin, cholesterol and protein) act on fats
  • Pancreatic lipases breakdown to

=monoglcerides/fatty acids and glycerol/fatty acids transported via the portal vein or thoracic duct

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46
Q

What are the functions of the exocrine pancreas?

A

Secretion of digestive juices into the GI tract via ducts

  • Neutralizes acidic chyme entering the duodenum from the stomach
  • Produces enzymes: proteases, amylases, and lipases
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47
Q

How does the pancreas protect itself from auto digestion by its own enzymes?

A

All proteases are secreted in their INACTIVE (aka pro-enzyme) form. Trypsin inhibitor is also produced

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48
Q

What are the functions of the endocrine pancreas?

A

Produces and secretes hormones into the vascular system

Insulin, Glucagon, Somatostatin

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49
Q

The Islets of Langerhans of the endocrine pancreas are made up of three types of cells. What are they are what do they produce?

A
  1. Alpha- Glucagon (converted to glucose)
  2. Beta- Insulin (glucose uptake)
  3. Delta- Somatostatin (inhibits alpha/beta)
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50
Q

What is dysphagia and what type of obstructions could it be related to?

A

Difficulty swallowing d/t mechanical or functional obstructions

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51
Q

What is GERD?

A

Reflux of acidic chyme from the stomach into the esophagus. Should be inhibited by LES

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52
Q

What is a blocking or narrowing of the opening between the stomach and the duodenum?

A

Pyloric obstruction

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53
Q

What does an ileus describe?

A

Failure of normal intestinal motility in the absence of an obstructing lesion

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54
Q

What state could cause natural decrease in the resting pressure of the LES?

A

Pregnancy (d/t high progesterone)

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55
Q

How can pregnancy predispose an individual to the development of gallstones?

A
  • High progesterone causes an increase in residual volume in the gallbladder causing bile stasis.
  • Estrogen
  • Down-reg of contractile G proteins in the gallbladder muscle impairs emptying
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56
Q

What is alchalasia?

A

Denervation of the smooth muscle in the esophagus and LES (causes dysphagia)

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57
Q

What could the constant irritation of the esophagus like in GERD predispose an individual to?

A

Cancer

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58
Q

What is Barrett Esophagus?

A

Complication of chronic GERD.
Columnar tissue replaces the normal squamous epithelial cells of the distal esophagus

(Significant cancer risk)

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59
Q

What is a hiatal hernia and what is the most common type?

A

A defect in the diaphragm that allows a portion of the stomach to pass through the diaphragmatic opening into the thorax

95% sliding hiatal hernia

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60
Q

What is a sliding hiatal hernia?

A

Portion of the stomach and gastroesophageal junction slip into the thorax (gastroesophageal junction is above diaphragmatic opening)

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61
Q

What is a paraesophageal hernia?

A

A part of the greater curvature of the stomach rolls through the diaphragmatic defect

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62
Q

What are herniations of the mucsosa of the colon through muscle layers of the colon wall (esp. sigmoid colon)?

A

Diverticula

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63
Q

What are the two stages of disease involving diverticula?

A

Diverticulosis- asymptomatic
Diverticulosis- inflammatory state
(pain, diarrhea, constipation, fever, leukocytosis)

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64
Q

What is a volvulus?

A

Twisting of the bowel on itself causing intestinal obstruction and blood vessel compression

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65
Q

What is the telescoping or invagination of a portion of the bowel into an adjacent portion called?

A

Intussusception

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66
Q

What is seen with high vs. low intestinal obstructions?

A

(d/t loss of water and lytes)
Alkalosis with high obstruction
Acidosis with low or late obstruction

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67
Q

What are inflammatory markers present in IBS?

A
  1. CRP
  2. Calprotectin (WBC)
  3. ESR
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68
Q

What is Kwashiorkor?

A

d/t starvation or malnutrition

Lack of proteins causes liver to swell d/t to the inability to produce lipoproteins for cholesterol synthesis

69
Q

What is Marasmus?

A

d/t starvation or malnutrition

Liver function continues but overall caloric intake is too low to support cellular protein synthesis resulting in a deficiency of ALL nutrients

70
Q

What is osmotic diarrhea?

A

Increased amounts of poorly absorbable solutes in the bowel that cause Na and H2O influx into the bowel lumen resulting in diarrhea
(Golytely)

71
Q

Diarrhea d/t a pathophysiologic event like the presence of a bacterial toxin causing active secretion and inhibiting resorption, is termed:

A

secretory diarrhea

Ex-cholera

72
Q

What is motility diarrhea related to?

A

Decreased contact time of chyme with the absorptive surfaces of the intestinal lumen (surgery, hyperthyroidism)

73
Q

What is peptic ulcer disease?

A

Break or ulceration in the protective mucosal lining of the lower esophagus, stomach and duodenum
Due to pepsin and HCl

74
Q

What is the most common peptic ulcer?

A

Duodenal ulcers

75
Q

What are duodenal ulcers related to?

A
  • *H. pylori infection (95-100% toxins/enzymes that promote inflammation and ulceration)
  • Hypersecretion of stomach acid
  • NSAIDs
  • Alcohol
  • Cigarettes (increase acid production)
  • Increased mass of gastric parietal cells, rapid gastric emptying, decreased duodenal bicarb production
76
Q

Which ulcer predisposes an individual to gastric cancer?

A

Gastric ulcer (esp w/ chronic H.pylori infection)

77
Q

What are gastric ulcers related to?

A
  • H. pylori (60-80%)
  • NSAID
  • Alcohol
  • Cigarettes
  • Zollinger-ellison syndrome(gastrin secreting tumor of the pancreas)
78
Q

How does the stress of critical illness increase a person risk for peptic ulcer disease?

A

Splanchnic hypoperfusion

79
Q

The stress ulcers, Curling and Cushing are d/t:

A

Curling: burn injury
Cushing: elevated ICP

80
Q

What is gastritis?

A

An inflammatory disorder of the gastric mucosa.

Acute gastritis: H.pylori, NSADIS

81
Q

What are esophageal varices d/t, who are they most common in, and what is their biggest risk?

A
  • d/t impaired hepatic blood flow
  • alcoholic cirrhosis
  • rupture and death
82
Q

What can pancreatic insufficiency be d/t and what is the main problem secondary to it?

A
  • Pancreatitis, carcinoma, pancreatic resection, and CF

- Fat maldigestion is the main problem (fatty stool, weight loss)

83
Q

Describe lactase deficiency:

A

Inability to break down and absorb lactose. Leads to fermentation of lactose by bacteria: cramping, osmotic diarrhea.

84
Q

Gluten-sensitive enteropathy is also known as:

A

Celiac Disease

85
Q

What is the patho of celiac disease?

A
  • T cell mediated autoimmune injury the villious epithelium in the small intestine
  • Gluten acts as a toxin
  • Abs produced are: tTG, EMA, DGP
86
Q

Inflammatory Bowel Disease refers to what two specific disease?

A

Ulcerative Colitis

Crohn Disease

87
Q

What mucosa is associated with inflammatory process of UC?

A

Sigmoid colon and rectum

88
Q

What is the etiology of UC?

A

Infectious
Immunologic (anticolon antibodies)
Dietary

89
Q

What are the symptoms of UC?

A

Diarrhea 10-20stools/day
Bloody stools
Cramping

90
Q

What is the treatment of UC?

A

Broad-spectrum antibiotics
Steroids
Immunosuppressive agents
Surgery

91
Q

T/F: UC and Crohn disease both have increased risk of colon GI cancer?

A

True

92
Q

What is one major difference between UC and Crohn disease?

A

UC affects are contiguous in the colon and Crohn disease affects any part of the GI tract via skip lesions

93
Q

How do ulcerations in Crohn disease affect the lympathics?

A

Ulcerations can produce longitudinal fissures that extend into the lymphatics

94
Q

S/S of Crohn disease:

A

Similar to UC
Less common bloody stools
R lower quadrant pain and possible mass

95
Q

Can UC or Crohn disease lead to fistula and abscess formation?

A

Crohn

96
Q

Inflammation and ulceration occurs where in UC vs Crohn?

A

UC: mucosal layer
Crohn: Entire intestinal wall

97
Q

T/F: Crohn disease can be related to family history?

A

True

98
Q

Where is pain felt with appendicitis and what is the greatest risk associated with it?

A

R lower quadrant

Peritonitis

99
Q

What is Hirschsprung Disease?

A

Congenital d/o of the large intestine
Parasympathetic nerve ganglia in the smooth muscle are absent or markedly reduced

Associated with Downs
Require lavage and surgery

100
Q

What is hepatitis?

A

Inflammation of the liver parenchyma (functional component of the liver)

101
Q

What are the 4 phases of hepatitis?

A
  1. Incubation
  2. Prodromal (preicteric) phase- ~2wks after exposure, variety of s/s ending with jaundice
  3. Icteric phase- acute phase; hepatocellular destruction and bile stasis
  4. Recovery- 6-8wks after exposure
102
Q

Hepatitis A: Transmission, Incubation, Immunity, Risk Factors

A

RNA virus

Fecal-oral transmission

2-7/4-6wks

Immunity: anti HAV IgG
Acute infection: anti HAV IgM

Unsanitary condition, food/water contamination

103
Q

Hepatitis B: Transmission and Ab development

A

Partially double stranded DNA

Infected blood, body fluids, contaminated needles
Maternal/baby in 3rd trimester
HepB vaccine prevents transmission

3 ypes of Ab particles develop against specific part of virus-differentiate

104
Q

Hepatitis C: Transmission, chronic liver disease, predisposition

A

Posttransfusion, IV drug use

50-80% of cases result in chronic liver disease

Cirrhosis could predispose patient to liver cancer

105
Q

Hepatitis D:

A

Incomplete viral organism that requires HBV for replication. Transmitted by blood/body fluids.

106
Q

How are HAV and HEV similar?

A
  • Self-limiting
  • 2-8wks incubation
  • Do NOT cause carrier state
  • Do NOT cause chronic hepatitis
  • Do NOT cause cancer
  • Oral transmission
  • Not common in US
107
Q

How are HBV , HCV, HDV similar?

A
  • Cause carrier state
  • Cause chronic hepatitis
  • Cause cancer
  • Close personal contact transmission
  • Present in US
108
Q

Why are serum markers helpful in diagnosing HBV, HCV, HDV?

A

Intracellular (hepatocyte) enzymes that have spilled into the extracellular space d/t damage (AST, ALT)

109
Q

Chronic hepatitis definition and causes:

A

Inflammation of the liver for 6months or more

Causes: Autoimmune disease, HBV, HCV, Toxins, metabolic disease

110
Q

S/s of chronic hepatitis:

A 
Fatigue, malaise
Nausea, anorexia
Ascites
Hepatomegaly
Abd. pain
Jaundice
111
Q

Alcoholic Hepatitis is active inflammation of what region of the liver?

A

Centrilobular

112
Q

What are Mallory bodies?

A

Present in alcoholic hepatitis.

Hepatocyte necrosis with neurophilic infiltration and intracellular inclusions

113
Q

Diagnosis of alcoholic hepatitis:

A

AST (SGOT) markedly >ALT (SGPT) shows toxic etiology rather than viral hepatitis

114
Q

What is bilirubin a breakdown product of?

A

Heme

115
Q

When old red blood cells pass through the spleen what happens?

A

Macrophages break the Hgb into Heme and Globin. Globin, an amino acid, is reabsorbed by the body. Heme is broken down into Iron which is reabsorbed and unconjugated bilirubin which is sent to the liver

116
Q

What does unconjugated bili (not water soluble) bind to to travel to the liver?

A

Albumin (complex is water soluble)

117
Q

What happens once the unconjugated bili arrives in the liver?

A

Hepatocytes conjugate it with glucoronic acid to produce water soluble conjugated bili.
It is then secreted into bile and the small intestine

118
Q

What could an increase in unconjugated bilirubin be indicative of?

A

Hepatocyte/liver dysfunction

119
Q

What could an increase in conjugated bilirubin be indicative of?

A

Obstruction distal to the liver

120
Q

Irreversible end state of many hepatic injuries:

A

Cirrhosis

121
Q

What is characteristic of cirrhosis?

A
  • Decreased hepatic function d/t nodular regeneration and fibrosis
  • Biliary channels become obstructed causing portal HTN-> blood shunted away from the liver =hypoxic necrosis
122
Q

Why does a ‘fatty liver’ develop in a patient with alcoholic cirrhosis?

A

More fat is delivered to the hepatocyte than it can metabolize or by a defect in fat metabolism within the cell

123
Q

What is biliary cirrhosis the end result of?

A

Continuous ongoing inflammation of bile ducts caused by biliary obstruction with bile backup into the liver

124
Q

What is primary biliary cirrhosis?

A

Autoimmune

  • Destruction of intrahepatic ducts, portal inflammation, and fibrosis
  • Mitochondrial IgG Abs, increased serum alkaline phosphotase, hyperbilirubinemia
  • Rule out gallstones, biopsy
  • Treat with corticosteriods or transplant
125
Q

What is secondary biliary cirrhosis?

A

Obstruction

  • Prolonged complete or partial blockage
  • Gallstones, tumors, fibrotic strictures
  • Increase pressure in hepatic bile duct
  • Mitochondrial IgG Abs, increased serum alkaline phosphotase, high conjugated bili
  • Surgery, endoscopy
126
Q

What is the function of bile?

A

Aids in digestion

Transports waste products (Bili, IgA, toxins, cholesterol)

127
Q

What is the function of bile salts?

A

Digestion
Absorption of fats from small intestine
Micelles that surround hydrophobic lipids and allow them into solute

128
Q

What is the most common type of cholelithiasis?

A

Cholesterol

129
Q

Patho of cholelithiasis:

A

Supersaturation of cholesterol, nucleation of crystals, hypomitility/bile stasis
(decreased fluid)

  • Enzyme defect in cholesterol synthesis
  • Decreased secretion of bile acids to emulsify fat
  • Decreased resorption of bile acids from ileum
  • Gallbladder smooth muscle hypomotility and stasis
  • Genetic predisposition
130
Q

S/s of cholelithiasis:

A

Biliary colic (persistent epigastric pain or R upper quadrant pain)
Colic d/t gallstones in the cystic or common duct (jaundice)
Intolerance of fatty foods

131
Q

Risk factors for cholelithiasis:

A 
Women 
Native American (highest risk)
Obesity
Rapid weight loss
CF and Sickle cell anemia
132
Q

Sties of common cholelithiasis obstruction include:

A

Cystic duct

Common bile duct

133
Q

What are pigment stones?

A

25% of gallstones
Black: bili and Ca salts (cirrhosis and hemolysis)
Brown: infectious processes

134
Q

What is pancreatitis?

A

Inflammation of the pancreas

135
Q

What are common causes of pancreatitis?

A 
Duct obstruction (cholelithiasis, alcoholism)
Acinar cell injury (trauma, ischemia)
Defective intracellular transport (metabolic injury)
136
Q

What is the patho of pancreatitis?

A
  • Injury or damage to pancreatic cells and ducts leads to leakage of pancreatic enzymes into the pancreatic tissue
  • Autodigestion of pancreatic tissue and leakage into the bloodstream causing injury to blood vessels and other organs
137
Q

What is the hallmark sign of chronic pancreatitis?

A

Necrosis of the exocrine parenchyma followed by fibrosis (leads to calcification ad obstruction to flow of pancreatic juices)

138
Q

What lab values may be indicative of acute pancreatitis?

A

Elevated amylase and lipase
Leukocytosis, hyperlipidemia, and hypocalcemia

(if assoc with biliary disease or obstruction: bili and alkaline phosphotase will be elevated too)

139
Q

Insulin secretion is stimulated by_______

A

glucose

140
Q

Glucagon secretion is inhibited by_______

A

insulin

141
Q

What inhibits gastric motility by raising the threshold potential of muscle fibers?

A

Secretin

142
Q

What do the enterochromaffin-like cells in the stomach do?

A

Secrete histamine

143
Q

The most common intestinal blockage is:

A

Adhesions

144
Q

When and how is insulin secreted?

A
  • When there is an increase in circulating glucose in the blood (ex-post meal), GLUT-2 transporters on the surface of beta cells will open allowing the glucose to move down its concentration gradient into the cell.
  • Once inside the cell glucose activates ATP which in turn opened ATP sensitive potassium channels.
  • The influx of potassium depolarizes the cell, increasing its positive charge. The increased in charge causes voltage gated Ca channels to open.
  • Ca rushes into the cell and activates insulin storage granules.
  • Via exocytosis the insulin is released out of the cell
145
Q

What are all diabetic conditions associated with?

A

Glucose intolerance

146
Q

What promotes secretions of insulin?

A

Chemical: increased glucose levels, amino acids, and serum free fatty acids
Hormonal: GI hormones
Neural: Parasympathetic stimulation of beta cells

147
Q

What inhibits the secretion of insulin?

A

Chemical: Decreased glucose levels and prostaglandin
Hormonal: Increased levels of insulin (neg feedback)
Neural: Sympathetic stimulation of alpha cells

148
Q

What is characteristic of Type 1 Diabetes?

A

Autoimmune destruction of beta cells

Type IV hypersensitivity

149
Q

What is characteristic of Type 2 Diabetes?

A

Insulin resistance

150
Q

What does GLUT 4 do?

A

Stimulated by insulin it allows glucose to enter the cell

151
Q

What are potential causes of Type 2 Diabetes?

A

Obesity
Genetic predisposition
Physical inactivity

causes pancreatic beta cell apoptosis and decreased insulin

152
Q

Why is increased blood insulin seen initially in Type 2 diabetics?

A

The body is attempting to lower blood glucose

153
Q

What is the Soymogi effect seen in diabetics?

A

Hypoglycemia followed by rebound hyperglycemia

More common in type 1

154
Q

What is the Dawn phenomenon seen in diabetics?

A

Early morning rise in blood glucose concentration with no preceding hypoglycemia
R/t to elevated elevations of GH

155
Q

What is DKA?

A

Primarily Type 1
Occurs as a result of lipolysis and conversion to ketone bodies. Excessive ketones result in metabolic acidoses decreased pH and bicarb levels. Acidosis induced hyperkalemia (followed by hypokalemia as body rids K in urine) and compensatory hyperventilation (Kussmaul resp) result in decreased CO2 and alkalosis.

156
Q

What is hyperosmolar hyperglycemic nonketotic syndrome? (HHNKS, HONKS)

A

Primarily Type 2
Severe hyperglycemia with no or slight ketosis and striking dehydration
Relative insulin deficiency

157
Q

What are AGE’s

A

Advanced Glycosylation End Products
Result from longterm hyperglycemia.
Glucose binds irreversibly to proteins in the body (ex-collagen in blood vessels).
Causes inflammatory process

158
Q

What does fasting blood glucose indicate and what is the normal range?

A

70-120mg/dL

Current snapshot of patients BG control

159
Q

What does HgA1C indicate and what is a normal range?

A

5-7%

Gives an accurate history of blood glucose control over the past 3months

160
Q

What does HgA1C represent?

A

Glucose and Hgb react to form a stable glyosylated Hgb product. The hight the blood glucose the more glycosylated Hgb is formed.

161
Q

What is high HgA1c closely associated with?

A

Micro-vascular and nerve complications

162
Q

Diabetes is the leading cause of ________ and _______

A

Kidney failure
~30% of patient will develop nephropathy
Retinopathy

163
Q

______ associated with diabetes is what leads to kidney failure.

A

HTN

164
Q

What is proliferative diabetic retinopathy?

A

Late stage; circulation attempts to maintain adequate oxygen levels by developing new, fragile vessels which hemorrhage easily

165
Q

What is peripheral neuropathy?

A

Pain or loss of feeling in the toes, feet, legs, arms, and hands
Blisters and sores develop on numb areas that go unnoticed
May lead to infection that could spread to the bone eventually needing amputation

166
Q

What is autonomic neuropathy?

A

Changes in digestion, bowel and bladder, sexual response, and perspiration. Can also affect the heart and BP control

167
Q

What is focal neuropathy?

A

Sudden weakness of one nerve or a group of nerves causing weakness or pain.

168
Q

Glycosuria puts a diabetic patient at risk for:

A

Water deficit

169
Q 
Type 1 diabetes can lead to:
muscle wasting d/t\_\_\_\_\_\_\_
ketoacidosis d/t \_\_\_\_\_\_\_\_\_
polyuria d/t \_\_\_\_\_\_\_\_\_
dehydration(DKA) d/t \_\_\_\_\_\_\_\_
A

increased protein catabolism
increased lipolysis
ketogenesis
glycosuria

Advanced Pathophysiology (12 decks)

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