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GIGU Exam 1 > Physiology Clinical Notes > Flashcards

Physiology Clinical Notes Flashcards

1
Q

Achalasia

A
  • Impaired peristalsis
  • Incomplete lower esophageal sphincter (LES) relaxation during swallowing – results in back-up of food
  • Elevation of LES resting pressure
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2
Q

Achalasia: Causes

A
  • Decreased numbers of ganglion cells in myenteric plexus
  • Degeneration preferentially involves inhibitory neurons producing NO / VIP
  • Damage to nerves in the esophagus, preventing it from allowing food in the stomach
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3
Q

Achalasia: Symptoms

A
  • Backflow of food in the throat (regurgitation)
  • Difficulty in swallowing both liquids and solids (dysphagia)
  • GERD
  • Chest pain
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4
Q

GERD

A
  • Occurs when there are changes in the barrier between the esophagus and stomach
  • Persistent reflux and the resulting inflammation lead to this condition
  • Backwash of acid and pepsin into the esophagus leading to heartburn and acid regurgiation
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5
Q

GERD: Causes

A
  • Motor abnormalities that result in abnormally low pressures in the LES
  • Increase in Intragastric pressure – commonly occurs after a meal, during heavy lifting, or during pregnancy
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6
Q

GERD: Complications

A
  • GI bleed
  • Irritation of the lining of the esophagus (esophagitis)
  • Scar tissue in the esophagus (stricture of esophagus)
  • Barrett’s esophagus
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7
Q

___ ___ ____ is the most common problem associated with disorders of gastric motility

A

Slow Gastric Emptying

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8
Q

Slow Gastric Emptying: Symptoms

A
  • Fullness
  • Loss of appetite
  • Nausea
  • Vomiting
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9
Q

Slow Gastric Emptying: Causes

A
  • Gastric Ulcer (scar tissue)
  • Cancer (physical obstruction)
  • Eating disorders (anorexia, bulimia, obesity)
  • Vagotomy
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10
Q

Gastroparesis

A

Slow emptying of stomach / paralysis of stomach in the absence of mechanical obstruction

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11
Q

Gastroparesis: Causes

A
  • Diabetes Mellitus
  • Injury to Vagus Nerve
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12
Q

Gastroparesis: Symptoms

A
  • Nausea
  • Vomiting
  • Early feeling of fullness when eating
  • Weight loss
  • Abdominal bloating
  • Abdominal discomfort
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13
Q

Chronic Constipation

A

Generally results from inadequate fiber or fluid intake, or from disordered colonic transit or anorectal function

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14
Q

Disordered Colonic Transit or Anorectal Function can be the result of:

A
  • Neurological disorders
  • Outlet obstruction to defecation
  • Certain drugs (ex. Opioids inhibit gastric emptying and peristalsis, and increase anal sphincter tone which impairs the defecation reflex)
  • Advanced age
  • Systemic diseases that affect GI tract
  • Metabolic disorders (ex. hypothyroidism, hypercalcemia)
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15
Q

Hirschsprung Disease: Cause

A

Ganglion cells absent from segment of colon; often present at birth

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16
Q

Hirschsprung Disease: Result

A

VIP levels low –> smooth muscle constriction / loss of coordinated movement –> colon contents accumulate

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17
Q

Hirschsprung Disease: Newborn Symptoms

A
  • Difficulty in passing stool (congenital megacolon)
  • Failure to pass meconium
  • Poor feeding
  • Jaundice
  • Vomiting
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18
Q

Hirschsprung Disease: Adolescent Symptoms

A
  • Constipation
  • Swollen belly
  • Malnutrition
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19
Q

Hirschsprung Disease: Treatment

A

Surgical resection of colon segment lacking ganglia

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20
Q

Cirrhosis

A
  • Chronic liver disease in which normal liver cells are damaged and replaced by scar tissue
  • Often caused by excessive alcohol intake
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21
Q

Alcohol misuse leads to accumulation of ___ within _____

A
  • Fat
  • Hepatocytes
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22
Q

Fatty Liver leads to ___

A

Steatohepatitis

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23
Q

Steatohepatitis

A

Fatty liver accompanied by inflammation, which often leads to scarring of liver and cirrhosis

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24
Q

Portal Hypertension

A
  • Can be caused by liver cirrhosis
  • Develops when there is resistance to portal blood flow, which most often occurs in the liver
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25
Q

Esophageal Varices

A

Swollen connections between systemic and portal systems at inferior end of esophagus

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26
Q

Caput Medusae

A

Swollen connections between systemic and portal systems around umbilicus

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27
Q

How can Liver dysfunction lead to Hepatic Encephalopathy?

A

(1) Decreased hepatic urea cycle metabolism in the liver due to cirrhosis or portosystemic shunting
(2) Accumulation of ammonia in systemic circulation
(3) Ammonia crosses BBB which results in increased brain water, direct neuronal toxicity, increased intracranial pressure, and altered neurotransmission

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28
Q

Jaundice (Icterus)

A
  • Occurs due to hyperbilirubinemia
  • Yellow pigmentation of the sclera, skin and mucous membranes
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29
Q

Hemolytic Anemia

A
  • Form of anemia due to hemolysis (RBC destruction)
  • Can lead to increased production of bilirubin – increased bilirubin level overwhelms liver’s capacity to produce conjugated bilirubin, resulting in increased unconjugated bilirubin
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30
Q

Physiological Neonatal Jaundice

A
  • Due to increased un-conjugated bilirubin in the blood during the first week
  • Typically resolves within the first 1-2 weeks after birth, depending on the maturation rate of bilirubin clearance systems
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31
Q

Physiological Neonatal Jaundice: 2 Main Causes

A

(1) Bilirubin production is elevated because of increased breakdown of fetal RBCs; shortened lifespan of fetal RBCs
(2) Low activity of UDP-Glucuronosyltransferase (UGT)

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32
Q

Crigler-Najjar Syndrome

A
  • Increased levels of un-conjugated bilirubin in the blood
  • Related to mutations in the gene that codes for UDP-Glucuronosyltransferase
  • Two types
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33
Q

Crigler-Najjar Syndrome: Type 1 (CN1)

A
  • Very severe
  • No function of UDP-Glucuronosyltransferase
  • Often results in Kernicterus
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34
Q

Kernicterus

A
  • Form of brain damage that is caused by the accumulation of un-conjugated bilirubin in the brain and nerve tissues
  • Permanent neurological sequelae of bilirubin-induced neurologic dysfunction
  • Develops during the 1st year postnatal
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35
Q

Kernicterus: Major Clinical Features

A
  • Cerebral Palsy
  • Sensoryneural hearing loss
  • Gaze abnormalities
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36
Q

Small Intestinal Bacterial Overgrowth (SIBO)

A
  • Condition of colonic bacteria overabundance in the SI
  • MMC is important for cleansing debris in SI and prevention of this condition
  • Can result in impaired small bowel motility, nausea, anorexia, chronic diarrhea, and bloating
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37
Q

Crigler-Najjar Syndrome: Type 2 (CN2)

A
  • Less severe type
  • Less than 20% function of UDP-Glucuronosyltransferase
  • Less likely to develop Kernicterus
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38
Q

Treatment for Infants with Crigler-Najjar Syndrome

A

Phototherapy with blue light; works up until age 4 when the skin gets too thick and blocks light

39
Q

Treatment for Crigler-Najjar Syndrome

A
  • Blood transfusions (may help control amount of bilirubin in blood)
  • Oral calcium phosphate and carbonate (forms complexes with bilirubin in the gut)
40
Q

Treatment for Crigler-Najjar Syndrome Type 1

A

Liver transplant

41
Q

Treatment for Crigler-Najjar Syndrome Type 2

A

Phenobarbital (aids in conjugation of bilirubin)

42
Q

Phototherapy Treatment of Hyperbilirubinemia in Neonates

A
  • Can be done on any newborn with a total serum bilirubin > 21 mg/dL
  • Works through a process of isomerization that changes trans-bilirubin into the water-soluble cis-bilirubin isomer
43
Q

Gilbert Syndrome

A
  • Increased levels of unconjugated bilirubin in the blood
  • Relatively mild; recognized during adolescence; may have mild episodes of hyperbilirubinemia that occur when body is under physiological stress
  • Mutation in gene that codes for UDP-Glucuronosyltransferase
  • Decrease in UGT1A1 expression resulting in decrease in enzyme activity level (30% of normal enzyme activity)
44
Q

Dubin-Johnson

A
  • Increased levels of conjugated bilirubin in the serum without elevation of liver enzymes
  • Defect in the secretion of bilirubins across the canalicular membrane
  • Mutations in gene that encodes the Multi-drug Resistance-Associated Protein 2 (MRP2) – normally this protein transports bilirubin out of the liver cells and into bile
  • Mild jaundice throughout life; might not appear until puberty or adulthood
  • Liver has black pigmentation – result of an intracellular melanin-like substance
45
Q

Rotor Syndrome

A
  • Buildup of both unconjugated and conjugated bilirubin in the blood, but the majority is conjugated
  • Gene mutations that lead to abnormally short, non-functional Organic Anion-Transporting Polypeptides (OATP1B1 and OATP1B3 proteins) or an absence of these proteins – these proteins normally transport bilirubin and other compounds from blood into the liver so they can be cleared from the body
46
Q

Difference between Rotor Syndrome and Dubin-Johnson:

A

Liver cells are not pigmented in Rotor Syndrome; Liver has black pigementation in Dubin-Johnson

47
Q

Inherited Disorders of Bilirubin Metabolism: Increased Conjugated Bilirubin

A
  • Dubin-Johnson
  • Rotor Syndrome
48
Q

Inherited Disorders of Bilirubin Metabolism: Increased Unconjugated Bilirubin

A
  • Hemolytic Anemia
  • Crigler-Najjar Syndrome
  • Gilbert Syndrome
49
Q

Gallstones (Cholelithiasis)

A
  • Occur when there is excess of either bile pigment (bilirubin) or cholesterol
  • Pigment stones (black stones) are formed of bilirubin polymers and are typically formed due to hemolytic anemia
  • Insufficient secretion of bile salts or phospholipids into gallbladder or excess cholesterol secretion into bile
50
Q

Causes of Gallstones:

A
  • Too much absorption of water from bile
  • Too much absorption of bile acids from bile
  • Too much cholesterol in bile
  • Inflammation of epithelium
51
Q

Cholecystitis

A
  • Inflammation of the gallbladder
  • Most commonly due to obstruction of the cystic duct from cholelithiasis
  • Causes intermittent biliary pain
52
Q

Choledocholithiasis

A
  • Gallstones occluding the common bile duct
  • Patients may have jaundice and conjugated hyperbilirubinemia
53
Q

Cholestasis

A

Occurs when biliary ducts are blocked

54
Q

Cholangitis

A

Infection of the bile ducts

55
Q

Pernicious Anemia

A
  • Failure to secrete IF leads to this condition
  • Stomach does not produce IF; decreased B12 absorption
56
Q

Pernicious Anemia: Common Causes

A
  • Atrophic Gastritis – chronic inflammation of the stomach mucosa leads to loss of parietal cells
  • Autoimmune Metaplastic Atrophic Gastritis – immune system attacks IF protein or Gastric Parietal Cells
57
Q

Other causes of Pernicious Anemia or Insufficient Absorption of Vitamin B12:

A
  • Gastrectomy: loss of parietal cells
  • Gastric Bypass: exclusion of stomach, duodenum and proximal jejunum alters absorption of Vit. B12
  • Lack of Pancreatic Enzymes to digest Haptocorrin / B12 complexes
  • Lack of functional Terminal Ileum
58
Q

Zollinger-Ellison Syndrome

A
  • Large secretion of gastrin by duodenal or pancreatic neuroendocrine tumors (gastrinomas)
  • Leads to increased H+ secretion by Parietal Cells (high rates of secretion than Peptic Ulcer Disease)
  • Increased Parietal cell mass (trophic effect)
  • High gastrin level inhibits the absorption of Na+ and H2O by the small intestine – Secretory Diarrhea
  • Excessive H+ in the duodenum overwhelms the buffer capacity of HCO3- in pancreatic juice which creates an ulcer
59
Q

Zollinger-Ellison Syndrome: Low pH of Intestinal Contents

A
  • Inactivates pancreatic digestive enzymes
  • Interferes with the emulsification of fat by bile acids
  • Damages the intestinal epithelial cells and villi
  • Leads to maldigestion and malabsorption – both result in Steatorrhea
60
Q

Secretin Stimulation Test

A
  • Used in the diagnosis of Gastrin-secreting tumors
  • Under normal conditions, administration of secretin inhibits gastrin release
  • In gastrinomas, injection of secretion causes a paradoxical increase in gastrin release
61
Q

Peptic Ulcer Disease: Causes

A
  • Helicobacter Pylori infection
  • NSAIDs
62
Q

Peptic Ulcer Disease

A

Often the result of loss of protective mucosal barrier, excessive H+ and Pepsin secretions, or the combination of the two

63
Q

Peptic Ulcer Disease: Two Types

A
  • Gastric Ulcers
  • Duodenal Ulcers
64
Q

Gastric Ulcer

A
  • Decreased H+ secretion
  • Increased Gastrin levels (because of decreased H+ secretion)
  • Causes damage to protective barrier of gastric mucosa
65
Q

Duodenal Ulcer

A
  • Increased H+ secretion
  • Increased Gastrin levels (increases in response to a meal)
  • Increased parietal cell mass due to increased gastrin levels
66
Q

Cystic Fibrosis & the Pancreas

A
  • Mutations in CFTR – cAMP-activated Cl- channel in the apical surface of the Duct Cell
  • Some mutations are associated with a loss of HCO3- secretion
  • May lose ability to flush enzymes out of the duct cell (normally proteases are activated in the ducts and start “digestion” process of pancreas) with is associated with the trypsin inhibitor becoming overwhelmed
  • May lead to recurrent acute and chronic Pancreatitis
67
Q

Genetic Causes of Obesity

A
  • Leptin or Leptin Receptor Gene Deficiency
  • Melanocortin 4 Receptor Gene Mutation
  • Prader-Wili Syndrome
  • Proopiomelanocortin (POMC) Deficiency
68
Q

Leptin or Leptin Receptor Gene Deficiency: Symptoms

A
  • Early-onset severe obesity
  • Infertility (hypogonadotropic hypogonadism)
  • Hyperphagia infections
69
Q

Leptin or Leptin Receptor Gene Deficiency: Finding

A

Leptin

70
Q

Melanocortin 4 Receptor Gene Mutation: Symptoms

A
  • Early-onset severe obesity
  • Increased linear growth
  • Hyperphagia
  • Hyperinsulinemia
71
Q

Melanocortin 4 Receptor Gene Mutation: Finding

A

MC4R mutation

72
Q

What is the most common genetic cause of obesity?

A

Melanocortin 4 Receptor Gene Mutation – homozygous worse than heterozygous

73
Q

Prader-Wili Syndrome: Symptoms

A
  • Neonatal hypotonia
  • Slow infant growth
  • Small hands and feet
  • Intellectual disability
  • Hypogonadism
  • Hyperphagia leading to severe obesity – although these individuals have paradoxically elevated Ghrelin (would expect this to be low in obese individuals)
74
Q

Prader-Wili Syndrome: Findings

A

Partial deletion of chromosome 15 or loss of paternally expressed genes

75
Q

Proopiomelanocortin (POMC) Deficiency: Symptoms

A
  • Red hair
  • Obesity
  • Adrenal insufficiency due to ACTH deficiency
  • Hyperproinsulinemia
  • Hyperphagia
  • Pale skin
  • Cholestatic jaundice
76
Q

Proopiomelanocortin (POMC) Deficiency: Findings

A

Loss of function mutations of POMC gene

77
Q

Anorexigenic

A

Promotes satiety

78
Q

Anorexigenic Hormones

A
  • Insulin
  • CCK
  • Leptin
  • PYY
79
Q

Orexigenic

A

Promotes appetite

80
Q

Orexigenic Hormone

A

Ghrelin

81
Q

Anorexia Nervosa (AN)

A
  • Characterized by self-starvation and excessive weight loss
  • Patients can become severely malnourished and significantly emaciated, leading to endocrinological and cardiological dysfunctions, and abnormalities within the digestive, skeletal, and reproductive systems
82
Q

Restrive Eating Disorders

A
  • In patients with these disorders there are alterations of hormones related to the gut-brain axis
  • BAsal and Pulsatile secretion of leptin is reduced in association with reductions in fat mass
  • Ghrelin resistance appears to be a conducive factor to a restrictive diet
  • Elevated levels of PYY – might contribute to decreased nutrient intake and disordered eating psychopathology
83
Q

Obesity in humans is often associated with high ___ levels and failure to respond to exogenous ____ (___ ___)

A
  • Leptin
  • Leptin (Leptin Resistance)
84
Q

Cholesterol Lowering Drugs: Bile Acid-Binding Resins

A
  • Used in patients with hypercholesterolemia
  • Non-absorbable bile-acid binding resins such as Cholestyramine cause large increase in excretion of bile acid
  • Rate of bile acid synthesis is increase by induction of 7 alpha hydroxylase
  • Depletion of liver cholesterol pool
  • Increase in hepatic uptake of LDL cholesterol from circulation
  • Lower plasma cholesterol levels
85
Q

Chronic disturbance in bile salt metabolism leads to:

A

Malabsorption Syndromes (Steatorrhea) and deficiency in fat soluble vitamins

86
Q

Diseases of the Liver:

A
  • Hepatitis (inflammation of liver)
  • Jaundice
  • Viral Hepatitis A, Hepatitis B, and Hepatitis C
  • Alcohol-induced Hepatitis
  • Drug-induced Hepatitis
  • Liver Cirrhosis (result of chronic hepatitis; characterized by fibrosis of liver lobules)
87
Q

Diseases of the Liver Lead to:

A
  • Normally leaky basement membrane between endothelial cells and hepatocytes is replaced by high density membrane containing fibrillar collagen
  • Spaced between endothelial cells and fenestrations in plasma membrane are lost
  • Increased stiffness of hepatic vascular channels offers resistance to free flow of blood through liver; elevated intra-sinusoidal fluid pressure –> portal hypertension
  • Impairment of free exchange of material between hepatocytes and blood
88
Q

Lactose Intolerance

A
  • Failure to digests dairy carbs due to deficiency or dysfunction of lactase
  • Lactose that is not digested and absorbed draws water into the GI tract through osmosis resulting in Osmotic Diarrhea
  • Lactose is also converted into small chain fatty acids and fermented in gas and short chain FAs
89
Q

Protein Assimilation Disorders

A
  • Cystinuria
  • Chronic Pancreatitis
  • Congenital Trypsin Absence
  • Hartnup Disease
  • Cystic Fibrosis
90
Q

Protein Assimilation Disorders: Cystinuria

A
  • Defect in transport (SLC3A1) or absence of di-basic AA transporter (SLC7A9) — Cysteine, lysine, arginine, ornithine are not absorbed at the proximal tubule
  • Due to intestinal deficiency – AA secreted in feces/urine
91
Q

Protein Assimilation Disorders: Chronic Pancreatitis

A

Deficiency of pancreatic enzymes – lack of proteases (ex. Trypsinogen)

92
Q

Protein Assimilation Disorders: Congenital Trypsin Absence

A

Absence of Trypsin; all pancreatic enzymes are gone

93
Q

Protein Assimilation Disorders: Hartnup Disease

A
  • Cannot absorb neutral AA
  • Symptoms resemble pellagra (niacin deficiency)
  • Autosomal recessive genetic disorder (SLC6A19 gene, Na+ dependent neutral AA transporter)
  • Sxs: diarrhea, mood changes, neurological problems, red scaly skin rash, photosensitivity, short stature, urine samples with high excretion of neutral AAs (tryptophan) and by-products (serotonin)
94
Q

Protein Assimilation Disorders: Cystic Fibrosis

A
  • Cannot neutralize stomach acid; proteases don’t work
  • CFTR mutations associated with loss of HCO3- secretion
  • Cannot move enzymes from ducts
  • Can lead to acute and chronic pancreatitis

GIGU Exam 1 (14 decks)

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