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Exam 1 Flashcards

(335 cards)

1
Q

Submucosal plexus

A

Nerve plexus in GI tract, below mucosa

Regulates secretion

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2
Q

Myenteric plexus

A

Nerve plexus in GI tract between circular and longitudinal muscle

Regulate motility and smooth muscle contraction

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3
Q

Input to enteric plexi

A

From spinal cord - sympathetic and parasympathetic autonomics

Enteric inputs - proprio and chemoreceptors within mucosa/submucosa

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4
Q

Outputs from enteric plexi

A

Regulate function of GI tract

Secretion, motility

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5
Q

Sympathetic innervation of GI tract

A

Directly innervate pancreas, liver, gall bladder, vascular smooth muscle of feed arterioles

General inhibition, vasoconstriction

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6
Q

Parasympathetic innervation of salivary glands

A

7th and 9th cranial nerves

Increase motor/secretory function

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7
Q

Parasympathetic innervation of GI (not salivary)

A

Vagus

Secretion and motility

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8
Q

Gastrin: Stimulus, action

A

Stimulated by peptides, amino acids, stomach distention

Function: Stimulate acid secretion and GI growth

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9
Q

Secretin: Stimulus and action

A

Stimulus: Duodenal acidity

Action: Pancreatic bicarb secretion

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10
Q

CCK stimulus and action

A

Stimulus: Fatty acids, amino acids in intestine

Action: Gall bladder contraction, pancreatic enzyme secretion and growth

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11
Q

GIP: Stimulus and action

A

Stimulus: Glucose, fatty acids in intestine

Action: Insulin release

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12
Q

High levels of CCK stimulate…

A

Activates motility of stomach and closure of pyloric sphincter

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13
Q

Incretins

A

GIP

GLP

Insulin secretion, reduced glucagon secretion

GLP-1 inhibits gastric emptying

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14
Q

Gastrin and CCK family overall

A

Increase intracellular Ca in target cells

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15
Q

Secretin hormone family: Members and physiological function

A

VIP, GIP, GLP-1

Increase cAMP and AC activity

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16
Q

Hormone concentration and length of intestine relationship

A

Increased length along GI tract = more hormone

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17
Q

CCK primary location

A

Intestine

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18
Q

Gastrin primary location

A

Stomach antrum

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19
Q

Secretin cell primary location

A

Intestine

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20
Q

GIP secreting cell primary location

A

Intestine

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21
Q

GLP-1 secreting cell primary location

A

Small intestine and colon

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22
Q

Pancreatic polypeptide stimulus and action

A

Stimulus: glucose

Action: decrease pancreatic bicarb and enzyme secretion

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23
Q

Ghrelin

A

Stimulates appetite

Decrease insulin release

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24
Q

Motilin

A

Initiates or sensitizes gastric motility

Initiates or sensitizes intestinal motility

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25
Entero-oxyntin
Stimulate acid secretion
26
Enterogastrone
Inhibit acid secretion
27
Non adrenergic, non cholinergic neurotransmitters
GI modulating peptides released from nerve endings in neural plexi
28
NANC: VIP and Guanylin Nerve ending location and action
Location: Mucosa and muscle of gut, colon Action: SM relaxation, increase cAMP, activate NaCl and water secretion
29
NANC: GRPor bombesin Location and action
Location: gastric mucosa Action: gastrin release
30
NANC: Enkephalins Location and action
Location: Mucosa and muscle of gut Action: Sphincter muscle contraction
31
NANC: Supbstance P Location and action
Location: salivary glands Action: Secretion, enhance blood flow
32
NANC: CCK Location and Action
Location: Enteric and hypothalamic neurons Action: Inhibit propulsion, activate satiety
33
Somatostatin
Paracrine Stimulated by low pH (\<2-3) in pylorus Decrease gastrin secretion
34
Histamine
Paracrine Stimulate acid secretion Activate crypt fluid secretion in intestine and colon
35
Salivary glands in mouth
Parotid - fluid Sublingual - mucous Submandibular - mixed
36
Salivary composition
Water Ions Organic compounds
37
Organic compounds in saliva
a amylase - starch digestion (pH 7.0) lingual lipase - fat digestion (pH 4.0) Lysozyme - anti bacterial
38
Protective effects of saliva
I-, SCN- IgA Lysozyme Lactoferrin
39
Sympathetic stimulation of salivary glands
cAMP increase Release of proteins (digestive enzymes) Vasoconstriction so no water/fluid flow
40
Parasympathetic stimulation of salivary glands
Ca increase HCO3 and protein secretion Vasodilation - increased fluid flow
41
AcH effects on saliva
HCO3 and protein secretion
42
Substance P effect on salivary glands
Vasodilation and increased fluid flow
43
Cardiac glands
Proximal stomach Secrete mucus
44
Gastric (oxyntic glands)
Central 3/4 of stomach Secrete HCl, Pepsinogen, Intrinsic factor
45
Pyloric glands
Secrete mucus into stomach and gastrin into blood
46
Cells of gastric glands
Chief cells - Pepsinogen Mucus secreting cells - Mucopolysaccharides Parietal cell - HCL, IF
47
Mechanism of parietal cell HCl secretion
H/K ATPase H20 + CO2 -- CA --\> H2CO3 --\> H + HCO3 HCO3 pumped out of basolateral side through HCO3/Cl antiporter
48
Mechanisms of regulation for acid secretion
Parasympathetic --\> Ach --\> Increase Ca --\> HCl secretion Digested peptides/stomach distention/GRP --\> Gastrin --\> Increase Ca --\> HCl secretion Histamine --\> H2 receptor --\> cAMP --\> Potentiate HCL secretion Histamine constitutively active
49
Cephalic phase of acid secretion
Chewing, swallowing stimulus Vagus nerve --\> Parietal cell + G cell activation
50
Gastric phase of acid secretion
Stimulus - Gastric distention Local and vagovagal reflexes --\> Parietal, G cell
51
Intestinal phase of acid secretion
Protein digestion products in duodenum Activate intestinal endocrine cells
52
Enterochromaffin cells
Secrete Histamine Constitutively active cells, basal level
53
G cell and S cell
G cell: Vagus activation + protein digestion activation --\> secrete Gastrin S cell: Vagus activation + low pH activation --\> Inhibit G cell
54
Aphthous ULcers
Inflammatory lesions Association with Crohns/UC
55
Forms of candidiasis
Psudomembranous candidiasis (Thrush) Erythematous candidiasis Hyperplastic candidiasis
56
Thrush
Pseudomembranous candidiasis Superficial, gray to white inflammatory membrane Underlying erythematous inflammatory base layer Worsoned infection in immunosuppressed patients, if on antibiotics that destoy normal oral flora
57
Erythematous candidiasis
Red, raw looking lesion May evolve from pseudomembranous candidiasis Associated with inhaled steroids Appears on dorsum of tongue, loss of lingual papillae
58
Hyperplastic candidiasis
Nodular, plaque like White persistent plaque, does not wipe off
59
Treatment of oral candidiasis
Nystatin - topical use Fluconazole - Inhibit P450 and reduces sterol synthesis Caspofungin - Echinocandin, decrease cell wall synthesis
60
Leukoplakia
Oral, white patch that cannot be scraped off Not characterized as any other disease 5-25% can progress to SCC Tobacco = risk factor
61
Erythroplakia
Less common than leukoplakia, more serious Red, velvety lesion Atypical dysplastic lesion, highly prone to progress to SCC
62
Oral hairy leukoplakia
Lateral portion of tongue Associated with immune compromised patients Caused by EBV
63
Traditional SCC
Smokers, 60s, oral lesion that infiltrates locally before mets
64
HPV associated SCC
Expression of HPV E6 and E7 protein --\> inactivate p53 and RB --\> tumor growth
65
Sjogrens disease: Definition and symptoms
Autoimmune disease that destroys exocrine glands Associated with RA Joint pain, xerostomia, dry eyes
66
Sjogrens pathogenesis
Glandular cells present antigen to T cells --\> cytokine activation (IF-gamma, IL2) B cell activation
67
Pleiomorphic adenoma
Benign mixed tumor Most common tumor of Parotid gland Treat with surgical incision
68
Warthin tumor
Papillary cystoadenoma lyphomatosum Benign cystic tumor Parotid gland
69
Mucoepidermoid carcinoma
Most common malignancy of minor salivary glands Increased risk with radiation exposure Mucous and squamous cell portions
70
GERD definition and pathogenesis
Reflux of stomach acid into esophagus Decreased anti reflux, hiatal hernia, decreased gastric emptying
71
Clinical features of GERD
Dysphagia, heart burn, chest pain, hematemesis
72
Microscopic findings of GERD
Epithelial basal zone hyperplasia Eosiniphils, lymphocytes, neutrophils
73
GERD complications
Bleeding Strictures Barrets
74
Barrets Esophagus
Long standing GERD Squamous cells --\> columnar Presence of goblet cells increases cancer risk Adenocarcinoma
75
Eosinophilic Esophagitis
Food allergy main cause Eosinophils in esophagus Rings and furrows --\> can lead to stricture
76
Eosinophilic esophagitis treatment
PPI - reduce eosinophil recruitment Steroids
77
Infectious esophagitis most common etiology
HSV CMV
78
Cell types affected in HSV and CMV esophagitis
HSV - epithelial cells CMV - stromal cells
79
Inclusions in HSV and CMV
HSV - nuclear inclusion in multinucleated cells CMV - nuclear and cytoplasmic inclusions in single cells CMV has englarged cels (cytomegaly)
80
Location of viral cells relative to ulcer, HSV/CMV
HSV - Edge of ulcer CMV - base of ulcer
81
Portosystemic anastamoses
1. Umbilical 2. Esophageal 3. Retroperitoneal 4. Superior anal canal
82
Esophageal SCC
More common in underdeveloped countries No connection to BE Squamous dysplasia due to smoking/alcohol Middle 1/3 esohagus
83
Esophageal adenocarcinoma
More common in developed countries - obesity Related to BE Lower 1/3 esophagus/GE j(x)
84
H Pylori gastritis: Definition and types
Inflammation of stomach due to H Pylori infection Most common cause of chronic gastritis 1. Antrum 2. Pan gastritis
85
Antral gastritis
Increased acid secretion --\> duodenal ulcers
86
Pangastritis
Multifocal atrophc gastritis Decreased parietal cells --\> decreased acid --\> intestinal metaplasia --\> carcinoma
87
Sequelae of H pylori gastritis
1. Peptic ulcer disease 2. Gastric adenocarcinoma, intestinal type 3. MALToma
88
Autoimmune gastritis: Definition and pathogenesis
Autoimmune disease targeting H/KATPase of Parietal cell (CD4 T cells) Chief cell damaged because of inflamamtion
89
Characterstics of of autoimmune gastritis
1. Decreased parietal --\> decreased acid --\> disinhibition of gastrin cells --\> ECL proliferation --\> carcinoid tumor 2. Decreased IF --\> B12 deficiency --\> megaloblastic anemia 3. Decreased acid --\> decreased iron absorption 4. Intestinal metaplasia --\> Dysplasia --\> Adenocarcinoma
90
Peptic ulcer disease causes
1. H Pylori 2. NSAIDs 3. Smoking
91
Benign peptic ulcer characteristics
Sharp, punched out Clean base b/c acid digesting necrotic debris Normal rugae surroundings Acid digestion can go deep and cause severe bleed
92
Malignant peptic ulcer characteristics
Irregular shape Base contains necrotic debris Damage to surrounding rugae
93
Peptic ulcer disease characteristics
1. Bleeding 2. Perforation 3. Gastric outlet obstruction
94
Hypertrophic gastropathy types
1. Menetrier Disease 2. Zollinger Ellison 3. Hypertrophic hypersecreting
95
Menetrier Disease
Increased TGF-B secretion Diffuse hyperplasia of foveolar epithelium of body/fundus Hypersecretion of mucus --\> protein loss in mucus --\> peripheral edema Hypoplasia of parietal and chief cells Increased risk of adenocarcinoma
96
Zollinger Ellison syndrome
Gastrin secreting tumor --\> Hyperplasia of parietal cells/ECL cells --\> gastric carcinoid tumor Duodenal ulcers and chronic diarrhea
97
Hypertrophic hypersecretory gastriopathy
Parietal cell hyperplasia with hypogastrinemia
98
Gastric adenocarcinoma - Intestinal type
Gland forming tumor Arise from intestinal metaplasia/dysplasia WNT-B-catenin pathway Increased incidence in FAP
99
Gastric adenocarcinoma - diffuse type
Rare gland formation \>50% signet ring cells Diffuse b/c mutation in CHD1 --\> loss of E cadherin --\> cells fall apart Can metastasize to ovaries --\> Krukenberg tumor
100
Gastric Carcinoid Tumors
Autoimmune gastritis Zollinger ellison syndrome Endocrine cell hyperplasia
101
H Pylori triple therapy
PPI 2 antibiotics
102
Omeprazole
Proton pump inhibitor Activated in acidic environment Long acting
103
H2 antagonists
Specific therapy for acid related diseases, ie GERD Cimetidine, Ranitidine, Famotidine Decrease acid and pepsin secretion
104
Cimetidine
1st H2 antagonist Short duration of action Inhibits P450
105
Ranitidine, Famotidine, Nizatidine
H2 antagonists Treat GERD and peptic ulcer disease Longer duration, no anti androgenic effects
106
Types of antacids
NaHCO3 Ca-OH/HCO3 Mg-OH/HCO3 Al-OH/HCO3
107
Sodium Bicarb antacid: onset, duration, alkalosis, stool effect
Rapid onset Short duration Yes alkalosis No stool effect
108
Mg antacid: onset, duration, alkalosis, stool effect
Rapid onset Long duration No alkalosis Laxative
109
Ca antacid: onset, duration, alkalosis, stool effect
Intermediate onset Long duration No alkalosis Constipating
110
Al antacid: onset, duration, alkalosis, stool effect
Slow onset Long duration No alkalosis Constipating
111
Sucralfate
1. Complexes with proteins at ulcer site --\> protective layer 2. Decreases back diffusion of H ion 3. Binds to pepsin and bile salts
112
Primary GI site of viral disease
Terminal ileum
113
E coli enterocolitis
Water, food, meat source Shigatoxin producing E Coli --\> Hemolytic uremic syndrome
114
Intestinal TB
Cecal disease most common Necrotizing granluomatous inflammation Stricture formation is common
115
Crohns disease: Location and characteristics
Primarily small intestine (terminal ileum) Skip lesions, transmural inflammation, granulomas (60% cases)
116
Ulcerative Colitis
Mucosal disease, mainly in colon Predisposed to pre malignancy, higher incidence in UC
117
Celiac Sprue
Cell mediated immune reaction to gluten Atrophic villi in SI via T cell mediated epithelial destruction Flat epithelia, diffuse enteritis, inflammatory infiltrate
118
Tropical sprue
Post infectious sprue Bacterial overgrowth (E Coli, hemophilus) Epithelium and submucosa equalliy inflamed
119
Psuedomembranous COlitis
C. Diff overgrowth Shallow superficial ulcers, covered by fibrin, polys, bacteria All oral antibiotics except Vanco cause it
120
Acute vs chronic ischemic colitis
Acute: * Mesenteric artery thrombosis * Intestinal obstruction * Causes intestinal infarction and peritonitis Chronic: * Arteriosclerotic disease, bloody stool and pseudomembranes
121
Irritable Bowel Syndrome
Intermittent abdominal pain and diarrhea Stress precipitates symptoms No anatomic change NM dysfunction/immune disorders may cause it Symptomatic treatment
122
Shigella COlitis
G- bacteria, developing world Distal colon Superficial inflammation
123
Amebiasis of colon
12% of world infected 10% symptomatic, 80% only intestinal disease Cecum and sigmoid are resevoirs Entameba histolytica cysts = infectious Trophozite = destructive
124
Most common infectious agent associated with vomiting (not food poisoning)
Norovirus
125
Most common pathogen causing watery diarrhea
Rotavirus
126
Pathogen/etiologies of malabsorption
Low volume diarrhea, but prolonged Giardiasis Lactose intolerance Celiac
127
Dysentery: Description and patholgical agents
Inflammatory disease of colon Fever, low abdominal pain, bloody diarrhea Shigella, Amebiasis, E coli, C diff
128
Syndrome of food poisoning and pathagent/food
Vomiting - S Aureua, Bacillus cerues enterotoxins Paralysis - Botulinum Scombroid fish poisoning - heavily muscled fish Paresthesias - fish, shellfish Diarrhea - C Perfingens toxin in intestines
129
Cholera MoA
Cholera toxin upregulates cAMP --\> Cl secretion --\> significant water loss
130
Secondary peritonitis
Rupture/perforation of GI tract --\> fecal matter and bacteria spills into peritoneum --\> systemic sepsis --\> so not chill
131
Primary peritonitis (SBP)
Spontaneous bacterial peritonitis Ascites in peritoneum often due to chronic liver failure, immune defenses low Bacteria arrive via blood stream or translocation through intestinal wall Common cause: E Coli, Strep Pneumoniae
132
CAPD and peritonitis
Complication of Continuous Ambulatory Peritoneal Dialysis Infection occuring due to exposure of peritoneum during PD
133
Clinical presentation of liver disease patients
Systemic symptoms - fever, malaise, nausea, vomiting Jaundice Coagulopathy - inadequate production of coagulation factors Ascites Portal HTN
134
Location and ratio of aminotransferases
Liver: ALT \> AST Muscle: AST \> ALT
135
Aminotransferases and liver disease
Damage to hepatocytes (or myocytes) increases enzymes in blood (testable) Acute hepatitis - Markedly increased ALT/AST Alcholic liver disease: Increased AST/ALT
136
Alkaline phosphatase and liver disease
Liver injury --\> AP moved to plasma membrane --\> released into blood Elevations = bile duct injury or infiltrative liver disease
137
Hepatitis A: Virus type, mode of transmission, illness progression
RNA virus transmitted fecal-oral Age 2-6 usually asymptomatic Symptomatic infection 4 weeks after exposure: Fever, nausea, malaise, diarrhea --\> jaundice No chronic infection Vaccine available
138
Hepatitis B: Virus type, mode of transmission, disease progression
DNA virus transmitted vertically, body secretions, blood IV drug users, sexual - western world Vertically - Developing world Can be asymptomatic, cirrhosis, liver failure Chronic infection risk decreases with age (90% newborns, 5% adults) Vaccine available
139
Hepatitis C: Virus type, mode of transmission, disease progression
RNA virus transmitted through blood, IV sharing, transfusions Acute infection - asymptomatic Chronic infection 20-60% Chronic Hep C most common cause of cirrhosis and liver cancer in Western world No effective vaccine
140
Hepatitis D: Virus type, mode of transmission, disease progression
Defective RNA virus, can only infect people with Hep B Can acquire B and D at same time Can acquire D with chronic B --\> liver disease more active
141
Hepatitis E: Virus type, transmission, progression
RNA virus, fecal oral Developing world SImilar to Hep A, milder Pregnant women --\> hepatic failure
142
Hep A serologic testing
IgM - acute infection IgG - Resolved infection or imunized
143
Hep B serology: HBsAg negative anti-HBc negative anti-HBs negative
Susceptible
144
Hep B serology: HBsAg negative anti-HBc positive anti-HBs positive
Immune due to natural infection
145
Hep B serology: HBsAg negative anti-HBc negative anti-HBs positive
Immune due to HepB vaccine Vaccine only contains HBs antigen
146
Hep B serology: HBsAg positive anti-HBc positive IgM anti-HBc positive anti-HBs negative
Acutely infected
147
Hep B serology: HBsAg positive anti-HBc positive IgM anti-HBc negative anti-HBs negative
Chronically infected
148
Hepatitis C serology
HCV AB+ = carriers, past infection HCV RNA+ = Chronic carriers
149
Hepatitis D serology
HDV IgM + = positive acute HDV IgG + = Positive chronic OR past infection HDV RNA + = chronic
150
Hepatitis A-E treatment
HAV - supportive care, no effective anti virals HBV - Interferon alpha, nucleoside analog HCV - Protease inhibtor HDV - Interferon alpha HEV - Supportive care
151
Other causes of acute hepatitis
Acetaminophen Autoimmune hepatitis Shock HF
152
Other causes of chronic hepatitis
Autoimmune/sclerosing cholangitis/primary biliary cirrhosis Alcoholic liver disease Alpha methyldopa
153
Bacterial infections of liver primary cause
Biliary tract disease (stones causing cholangitis) Pyogenic abscesses
154
Characteristics of biliary tract disease
Jaundice Fever Colic pain Liver tests - ALP elevated
155
Treatment of biliary tract disease
Drainage of infected bile surgically of ERCP
156
Pyogenic liver abscess characteristics and diagnosis
Chronic fever CT/MRI, aspiration and culture of abscess material Treat with antibiotics
157
Bilirubin fractionation = mixed --\> ALP elevation = ?
Cholestatic disease Biliary tract disease Look for stones, abscess, tumors in biliary system
158
Bilirubin fractionation = mixed --\> AST/ALT elevation = ?
Hepatitis Serological testing
159
Bilirubin fractionation = most unconjugated, low elevation = ?
Hemolysis or Gilberts Physiological jaundice or Crigler Najjar
160
Replicative HBV serology
HBV DNA = High HBeAG = + Increased ALT
161
Non replicative HBV serology
HBV DNA low HBeAg - HBeAb +/- ALT normal
162
Agenisis of pancreas
Rare condition, complete absence of pancreas PDX1 gene
163
Pancreas Divisum
Most common congenital abnormality of pancreas Failure of fusion of fetal pancreatic duct system Predisposition to chronic pancreatitis
164
Annular pancreatitis
Portion of pancreas wraps around duodenum --\> obstruction
165
Ectopic pancreas
Normal pancreatic tissue present where it shouldn't be Jejunum, Meckel diverticulum, ileum
166
Acute pancreatitis definition
Reversible pancreatic parenchymal injury, associated with inflammation
167
Common causes of acute pancreatitis
Biliary tract disease Medication Infection (mumps) Alcohol Ischemic injury (shock, vasculitis, atheroembolism)
168
Pathogenesis of acute pancreatitis
1. Duct obstruction 2. Primary acinar injury 3. Defective intracellular transport of proenzymes
169
Acute panreatitis: Duct obstruction
Blockage of ductal system --\> retrograde intraductal pressure --\> Leakage of enzymes into pancreatic tissues --\> DESTRUCTION --\> cytokine infiltration and inflammation Inflammation and edema = compromised blood flow --\> more damage
170
Acute pancreatitis: Primary acinar injury
Secondary to alcohol, viruses, drugs, trauma, shock
171
Acute pancreatitis: Defective enzyme transport
Enzymes transported to where they shouldnt be --\> acinar cell damage
172
Alcohol and pancreatitis mechanisms
Increase sphincter of oddi contraction --\> stone obstruction Toxic effect on acinar cells Oxidative stress --\> fusion of lysosome and zymogen granules --\> damage to acinar cells
173
Hereditary pancreatitis
10-20% unknown etiology Recurrent attacks of severe pancreatitis in childhood Mutations in cationic trypsinogen gene
174
Histology of acute pancreatitis
Microvascular leaks --\> edema Fat necrosis via lipolytic enzymes Destruction of parenchyma Destruction of blood vessels
175
Clinical presentation of acute pancreatitis
Abdominal pain Epigastric tenderness Nausea/vomiting Fever Hypotension Subcutaneous fat necrosis
176
Lab evaluation of acute pancreatitis
Elevated serum/urine amylase Elevated lipase Hypocalcemia
177
Chronic pancreatitis definition
Inflammation of pancreas with irreversible destruction of exocrine pancreatic parenchyma, fibrosis ---\> endocrine parenchyma destruction
178
Causes of chronic pancreatitis
Most common: Chronic alcohol abuse Cystic fibrosis (duct plugging) Drugs, virus, shock, etc
179
Acute pancreatitis treatment
Rest IV fluids Pain meds
180
Pancreatic congenital cysts
Anomalous development of pancreatic duct Lined by uniform cuboidal epithelium Sporadic Syndromic - ADPKD, von Hippel Lindau
181
Pancreatic pseudocyst
Localized collection of necrotic/hemorrhagic material rich in pancreatic enzymes No epithelial lining Large Alcohol, traums
182
Serous cystadenoma
Benign cystic neoplasm, clear fluid 25% of cystic neoplasms in pancreas 70s Surgical resection
183
Mucinous cystic neoplasm
95% in women Associated with invasive carcinoma Painless slow growing mass, filled with mucin Evaluate for malignancy after removal
184
Intraductal Papillary Mucinous neoplasm (IPMN)
Mucin producing intraductal neoplasm, more in males Pancreatic head Involve large pancreatic duct
185
Solid pseudopapillary neoplasm
Young women LArge circumscribed, solid and cystic Neoplastic cells in sheets/papillary projections Activating mutation of B catenin
186
Pancreatic cancer
Infiltrating pancreatic ductal adenocarcinoma = 4th leading cause of cancer death Highest mortality rate Smoking, fat, chronic pancreatitis, diabetes, alcohol
187
Pancreatic intraepithelial neoplasia
Precursos of pancreatic cancer
188
Types of cholelithiasis
1. Cholesterol (80%), western 2. Pigment (20%), non western
189
Cholesterol stone pathogenesis
Cholesterol normally soluble in bile High cholesterol concentrations --\> precipitates out and forms crystals --\> crystals aggregate and form stones
190
Contributing factors to cholesterol stone formation
Biliary hypersecretion of cholesterol Gallbladder hypomobility - promotes nucleation Altered bile composition Mucus hypersecretion - traps crystals
191
Cholesterol stone risk factors
Native American Age Female Estrogen Obestiy Gallbladder stasis Fam hx FEMALE FAT FORTY FERTILE
192
Pigment stones: Composition and pathogenesis
Mostly bilirubin calcium salts INfection of biliary tract --\> release of beta glucoronidases --\> hydrolyze bilirubin glucoronides --\> bilirubin release Intravascular hemolysis --\> increased biliary excretion of conjugated bilirubin
193
Risk factors for pigment stones
Hemolytic syndromes Bacterial/parasitic infection of biliary tract
194
Cholesterol stone morphology
YELLOW Finely granular, hard external Radiolucent if pure cholesterol Radiopaque if mixed with Ca
195
Pigment stone morphology
Black - Sterile sites. Small, numerous, soft, radiopaque Brown - Infected bile ducts. Laminated, radiolucent
196
Cholesterolosis
Cholesterol esters accumulate within lamina propria
197
Acute Calculus Cholecystitis - Definition, presentation, labs, treatment
Most common complication Chemical irritation and inflammation caused by obstruction of gallbladder neck/cystic duct RUQ pain, fever, tachycardia Jaundice - bile duct obstruction Labs: Mild WBC increase, mild ALP increase Immediate surgery
198
Acute acalculus cholecystitis: Definition, signs/symptoms, prognosis
No gallstones, critically ill patients (surgery, trauma, sepsis, burns) Related to ischemia due to decreased flow through cystic artery Fatal if not recognized early
199
Chronic Cholecystitis
May or may not be associated with prior attacks \>90% associated with gallstones Recurrent RUQ pain, nausea, vomiting, intolerance for fatty foods
200
Acute cholescystitis complications
Empyema - Lumen filled with pus, gallbladder wall thickened, edematous, hyperemic Gangrenous cholecystitis - Necrotic gallbladder wall, prone to perforation Emphysematous cholecystitis - Gas in gallbladder due to gas forming organisms
201
Chronic cholecystitis complications
Porecelain gallbladder - dystrophic calcification within gallbladder wall Xanthogranulomatous cholecystitis - Shrunken nodular gall bladder, lipid laden histiocytes Hydrops - Atrophic, chronically obstructed gall bladder filled with clear secretions
202
Choledocolithiasis
Stones within biliary tree - 10% gallstone patients Symptoms from: Duct obstruction, pancreatitis, cholangitis, hepatic abscess
203
Cholangitis
Infection of bile ducts Spread into intrahepatic ducts = ascending cholangitis Suppurative cholangitis - purulent bile fills bile duct and extends to hepatic parenchyma --\> abscess
204
Commone cholangitis pathogen
Gram - bacteria E coli Klebsiella Bacteroides
205
Charcots Triad
Fever Jaundice RUQ pain CHOLANGITIS
206
Biliary atresia
Most common cause of death from liver disease in early childhood Rapidly progressive biliary cirrhosis Fatal at age 2 if not treated
207
Choledochal cysts
Congenital dilations of common bile duct Increased risk of bile duct carcinoma
208
Gall bladder carcinoma
Female predominance Stone/infections may be risk factors Poor prognosis, most are incidental findings Growth patterns: 1. Infiltrating - irregular, diffuse thickening of wall, firm 2. Exophytic - Irregular, cauliflower like mass growing into lumen
209
Extrahepatic bile duct carcinoma
Elderly patient with jaundice Risk factorsL Biliary tree infections, primary sclerosing cholangitis, IBD Poor prognosis
210
Amylose
Plants Linear alpha 1,4 bonds
211
Amylopectin
Amylose + 1,6 bond branches
212
Glycogen
Amylopectin + branches
213
Cellulose
Linear Beta 1,4 bonds
214
Mouth digestion
Salivary amylase Cleaves amylopectin
215
Sucrase-Isomaltase complex: Enzymes, substrate, product
Sucrase: Sucrose --\> Fructose+glucose Maltase: Maltose/Maltotriose --\> Glucose Isomaltose: A limit dextrins --\> glucose
216
Glucose/Galactose enterocyte absorption protein
SGLT1
217
Fructose enterocyte absorption
Glut5
218
Lipid Digestion Steps
Minor Digestion Major Digestion Bile acid Passive absorption Re esterification Assembly and export
219
lingual lipase: Action site, substrate, product
Mouth/stomach Substrate: TAG w/ medium chain FA Product: FFA + DAG
220
Pancreatic LIpase: Action site, substrate, product
SI lumen TAG with long chain FA FFA + 2MG
221
Phospholipase A2: Action site, substrate, product
SI lumen Phospholipids Unsaturated FFA + Lysolechthin
222
Lipoprotein Lipase: Action site, substrate, product
Capillary wal TAG in chylomicron of VLDL FFA + Glycerol
223
Insulin function
Promotoes anabolic processes Inhibit catabolic processes Counter regulatory to glucagon, epi, cortisol Stores glycogen, TAG, protein Increase AA/glucose transport into muscle and fat
224
Insulin production steps
1. mRNA production 2. Preproinsulin synthesized, uptake into ER, signal peptide cut 3. Proinsulin transported ot golgi 4. Proinsulin --\> insulin, C peptide removed 5. Insulin stored 6. Glucose --\> Ca contraction of microfilaments 7. Granule formation w/ membrane
225
Glucagon processing in pancreas
Preproglucagon --\> Proglucagon (signal peptide cut) --\> Glucagon (Golgi proteases)
226
Intestinal glucagon: Stimulus and processing
Stimulated by high AA Proglucagon --\> Glicentin + GLP-1 Increase insulin, decrease acid secretion
227
Glucose signaling
Glucose binds --\> metabolized --\> ATP activates Ca channels --\> Immediate Insulin secretion Glucose binds --\> metabolized --\> DAG activates PKC --\> Increase insulin synthesis
228
Insulin, Ca, Calmodulin
Calcium binds to calmodulin --\> CAM kinase activated --\> Increased insulin synthesis
229
Parasympathetic control of insulin
Ach --\> Increase insulin secretion via increased Ca and increased PKC
230
Sympathetic control of insulin secretion
Alpha2 receptors --\> decrease cAMP --\> decrease secretion Beta 2 receptors --\> increase cAMP --\> increase insulin secretion NET EFFECT: Decreased
231
Glucagon and GLP on insulin secretion
Both increase cAMP, small effect though Glucagon: Acts in concert with insulin for normoglycemia. fine tuning control GLP1: Active with AA's, increase insulin for increased AA uptake by liver for gluconeogenesis
232
Glucagon stimuli
Hypoglycemia - Most potent stimulus Promotes liver glucose formation: Glycogenolysis --\> gluconeogenesis Epinephrine increases secretion - fight or flight
233
Insulin and Glucagon response: Elevated blood glucose
Insulin: increase Glucagon: Decrease
234
Insulin and Glucagon response: Amino Acids
Insulin: Increased Glucagon: Increased
235
Insulin and Glucagon response: Ketones
Insulin: Increase Glucagon: No effect
236
Insulin and Glucagon response: GI Peptides
Insulin: increase Glucagon: No effect
237
Insulin and Glucagon response: SNS catecholamines
Insulin: Decrease Glucagon: Increase
238
Insulin and Glucagon response: Somatostatin
Insulin: decrease Glucagon: Decrease
239
Insulin actions
Synthesis/storage of glycogen, fats, TGs Activate capillary lipoprotein lipase Increase amount and activity of liver glucokinase Boost glycogen synthase activity Maintain protein balance
240
Insulin signal transduction
Insulin binds --\> 1st TyrK activated --\> 2nd TyrK phosphorylated --\> 1st TyrK phosphorylated --\> Activate Glut channels + Dephosphorylate metabolism enzymes
241
GLUT activation signal transduction
Active IRTK --\> Activate docking protein --\> p85/pI3K --\> PIP3 --\> PDK --\> PKB --\> Signals golgi to traffic GLUT4 to membrane
242
Metabolism inhibition via insulin
Active IRTK --\> PLC active --\> GPI to IPG --\> Active protein phosphatase --\> Dephosphorylate glycogen synthase, glycogen phosphorylase, phosphorylase kinase
243
Metabolic Syndrome
Potential risk to develop Type II DM and CV disease Glucose tolerance, obesity, HTN, HLD Insulin sensitivity common
244
Role of fatty acids and insulin sensitivity
Circulating fats induce resistance by replacing glucose as key fuel, alter downstream signaling
245
Proinflammatory cytokines and insulin sensitivity
Trigger inflammation associated with metabolic syndrome TNFa: Hypertriglyceridemia in obesity IL6: Increase hepatic output of VLDL Resistin: Prevents adipocytes from becoming larger, causes insulin resistance
246
Progression of type II DM
Insulin resistance --\> hyperglcemia --\> Hyperinsulinemia --\> increased pancreatic B cell demand --\> Decrease insulin response --\> Worse hyperglycemia --\> increased demand --\> Ultimate inadequate response
247
Type II DM inadequate insulin secretion? Glucose toxicity theory
Hyperglycemia --\> glucose toxicity Beta cells over taxed --\> under expression of GLUT 2, decreased glucokinase transcription, desensitization
248
Type II DM insulin inadequate: Lipotoxicity
Excess fats --\> lipotoxicity Obesity blunts glucose response Altered mitochondrial metabolism of pyruvate = decreased ATP Induction of uncoupling protein --\> decreased OxPhos
249
Lipotoxicity and amylin theory
Increased FA --\> amylin Amylin reduces post prandial glucagon secretion --\> diminish hepatic glucose output --\> Reduce hyperglycemia risk High fat diet --\> Increased amylin --\> Replace cell mass/barrier/reduce function/impair insulin secretion
250
Type I DM
Absolute deficiency of insulin secondary to auroimmune destruction of islet B cells Failure of tolerance to self Autoantibodies to B cells
251
Type II DM
Relative deficiency of insulin Inadequate secretory response by B cells in face of hyperglycemia Insulin resistance --\> B cell dysfunction
252
Advanced Glycosylation End Products
Form when nonenzymatic rxns occur between intracellular glucose and amino products, accelerated in hyperglycemia AGE receptor mediated events --\> proinflammatory cytokine release, ROS generation, proliferation of cascular endothelium and ECM AGE's can cross link to ECM --\> decreased vascular elasticity
253
DM and microvascular disease
Hyperglycemia activates PKC --\> VEGF production and neovascularization of diabetic retinopathy PKC increases vasoconstrictors and decreases dilators Proinflammatory cytokines and profibrogenic factors produced --\> Inflammation and increased BM deposition Glutathione production --\> increased susceptibility to oxidative stress
254
DM and macrovascular disease
Accelerated atherosclerosis in aorta and large/medium arteries MI due to infarction Hyaline arteriolosclerosis associated with HTN
255
Diabetic microangiopathy
Diffuse thickening of basement membranes Most evident in skin, skeletal muscle, retina, renal glomeruli, medulla Diabetic capillaries are leakier Underlies development of diabetic neuropathy, nephropathy, retinopathy
256
Diabetic nephropathy
Glomerular lesions, renal vascular arteriolosclerosis, pyelonephritis Capillary BM thickening Diffuse mesangial sclerosis
257
Nodular glomerularsclerosis
Nodules of matrix material present in glomerular periphery Hyalinosis of afferent/efferent arterioles
258
Type I DM Clinical features
Polyuria, polydipsia, polyphagia, ketoacidosis Insulin deficiency results in catabolic state with decreases assimilation of glucoe into cells Intracellular hyperosmolality = polydipsia
259
Ebb phase of shock: Definition and purpose
Early post trauma period of hypotension and decreased energy consumption Protective response within first 24hrs to maintain perfusion --\> inadequate perfusion so body switches to anaerobic metabolism --\> acidosis
260
Ebb phase hormonal changes
Increase in catabolic hormones: Glucagon, Cortisol, Epi Decrease in anabolic hormones: Insulin, sex hormones Protein metabolism, increase glyogenolysis, gluconeogenesis, lipolysis
261
Flow phase in shock: definition and purpose
Follows Ebb phase with proper resucitation Repair of damaged tissues, negative nitrogen balance, increased energy consupmtion Highly catabolic with increased protein degradation Hyperglycemia results b/c of peripheral insulin resistance of non damaged tissues
262
Strategy of care in Ebb phase
Treat cause of hypovolemic shock, stop progress of Ebb phase * Stop hemorrhage * Administer oxygen * Administer IV volume * Repair injury
263
Recovery phase treatment strategy
Multi team approach Prevent developing comlications Prevent hospital acquired infections Nutritional supplementation Strengthen therapy/rehabilitation
264
Fed state: Origin of glucose, tissues using glucose, brain fuel
Origin: Exogenous Tissues using glucose: All Brain fuel: Glucose
265
Post absorptive phase: Origin of glucose, tissues using glucose, brain fuel
Origin: Hepatic glycogen, gluconeogenesis Tissues: All except liver. Muscle/adipose at lower rates Brain fuel: Glucose
266
Early fasting phase: Origin of glucose, tissues using glucose, brain fuel
Origin: Gluconeogenesis Tissues using glucose: Brain and RBCs, small amount by muscle Brain fuel: Glucose
267
Prolonged starvation: Origin of glucose, tissues using glucose, brain fuel
Origin: Gluconeogenesis Tissues using glucose: Brain at diminished rate, RBCs Brain fuel: Ketone bodies
268
Brunners Glands
Mucus secreting glands in duodenum Protect against acid load coming from stomach
269
Crypts of Lieberkuhn
Located in crypts of small intestine Contain pluripotent stem cells for cell regeneration
270
Stimulus for intestinal stem cells
CCK
271
Active water secretion in intestine
cAMP activated CFTR protein, pumps out Cl Water follows Cholera mechanism
272
Normal inducer of intestinal active water secretion
VIP
273
Normal water flow in intestine
Water absorption and HCO3 secretion (Cl/HCO3 antiport)
274
Intestinal Na absorption
Majority occurs in jejunum (80%) 1. Na/H antiport 2. Na/substrate co transport 3. Na channel
275
Intestinal sodium absorption by location
Na/H: High in proximal intestine, low in colon Na/substrate co transport: Decrease along length of intestine Na channel: Most important in distal colon
276
Aldosterone in intestine
Increases number of Na channels --\> Regulate water absorption
277
Cl absorption
Proximal intestine: Paracellular to account for electrochemical gradient created by Na absorption Distal colon: Cl/HCO3 antiport. HCO3 neutralizes H created by bacteria
278
K absorption in intestine
Completely passive absorption Proximal - absorption b/c solvent drag Distal - No solvent drag, slower absorption, but driving force increased b/c water absorption = increased [K luminal]
279
Pathophysiology of diarrhea
1. Motility: Increased vs decreased propulsion 2. Absorption: Malabsorption disorders 3. Seretory: Cholera, VIPoma
280
Castor Oil
In low doses, induces crypt cell AC --\> opens Cl channels --\> laxative action
281
Magnesium sulfate
Osmotic laxative Not absorbed well because of charge --\> induce laxative action
282
Bulk forming laxatives
Bran, Psyllium, methylcellulose Contain non digestible fibers --\> cause motility and defecation reflex Safest and preferred
283
Loperamide
Opioid agonist Reduce motility and GI contraction
284
Diphenoxylate
Synthetic opioid w/ atropine to prevent abuse Overdose can cause respiratory depression (CNS stimulation)
285
Bismuth Subsalicylate
Anti diarrheal May bind bacterial toxins and prevent cAMP induced diarrhea
286
Cholestyramine
Binds bile acids and prevents diarrhea caused by inadequate bile acid uptake Chronic therapy can interfere with fat digestion --\> steatorrhea
287
Prokinetic drugs used for...
GERD Gastroparesis Refractory constipation
288
Dopamine and GI motility
Dopamine inhibits GI motility
289
Metoclopramide
Dopamine antagonist (5HT3) --\> Increase motility 5HT4 agonist, ganglionic stimulant --\> increase motility Prokinetic and anti emetic Crosses BBB --\> Sedation, anxiety, dystonic
290
Bethanechol
M2 agonist --\> Promote motility
291
Domperidone
Dopamine antagonist Ganglionic stimulant Prokinetic, antiemetic NO BBB CROSSING Headaches, gynecomastia
292
Baclofen
GABA agonist --\> Reduces LES relaxation CNS effects --\> Drowsiness, dizziness
293
Splanchnic circulation
ORgans fed by celic, SMA, IMA
294
Segmental control of alimentary blood flow
Regulated by tissue activity Distension/movement in region --\> increased motility and elevated blood flow
295
Transmural blood flow of alimentary canal
Blood flow to different intestinal layers is highest in those with most activity
296
Post prandial hyperemia
Blood flow to alimentary canal increases substantially floowing meal Buildup of metabolic end products --\> vasodilation to increase O2 availability and remove absorbed nutrients
297
Countercurrent exchange in intestinal villus
Oxygenated blood flow in and venous blood flow out of villus is parallel O2 flows from arteriole to venule down concentration gradient directly
298
Implications of villus countercurrent exchange
O2 delivery impeded, can lead to ischemic hypoxia Increased osmolarity as blood reaches tip which contributes to increased water absorption
299
Protective mechanisms in alimentary canal
HCl in stomach kills bacteria Ileal-Cecal sphincter - unidirectional flow MMC - Bacteria remains in colon but material removed from stomach/SI during inter digestive periods GALT - Dendritic cells and liver kuppfer cells
300
Factors affecting alcohol absorption
COncentration of alc Irritant properties of alc Type of beverage Blood flow to site of absorption Food Rate of ingestion
301
Food effect on alcohol
Food delays gastric emptying and slow absorption rate Food boosts rate of alcohol metabolism Return to zero alc concentration is earlier Hepatic first pass is greater
302
Alcohol Distribution
Distributed to tissues in proportion to H2O content Not absorbed by fats (women have more fat --\> higher BAC b/c not absorbed)
303
Alcohol first pass gastric metabolism
Mediated by gastric alcohol dehydrogenase Women lack this enzyme Low in alcoholics
304
Metabolism of alcohol
Alcohol --\> Acetaldehyde (ADH) --\> Acetate (Aldehyde dehydrogenase) Each step NAD --\> NADH
305
Cytochrome metabolism of alcohol
CYP2E1 metabolizes alcohol at BAC\>.08% Induced in chronic alcohol consumption
306
Genetic polymorphisms in alcohol metabolism
ADH isoforms can result in faster metabolism --\> lower risk for heavy drinking and alcohol problems ALDH variations (common in asians) --\> problems with aldehyde breakdown = severe reactions
307
Fomepizole
ADH inhibitor Used in management of methanol and toxic alcohol poisonings
308
Disulfiram
ALDH inhibitor Noxious effects due to increased aldehyde in blood
309
Metabolic effects of alcohol metablism
Increased NADH/NAD ratio Inhibits: Glycolysis, Krebs, PDH, LDH, Fatty acid oxidation
310
Metabolic consequences of heavy alcohol use
Hypoglycemia: Heavy drinking while fasting. Glycogen stores gone and Alc inhibits gluconeogenesis Ketonemia: Increase acetone formation and Acetoacetate --\> BhydroxyButarate b/c high NADH Lactic Acidosis: Increase lactate formation, LDH Hyperuricemia: Lactic acidosis competes with uric acid for renal tubular secretion --\> uricemia
311
Alcohol and lipid metabolism
Alcohol intake --\> Decreased NAD --\> Beta oxidation of fatty acids cannot be completed Increased NADH --\> Triglyceride synthesis --\> Hypertriglyceridemia
312
Acute molecular neuro effects of alcohol
Increased dopamine release Increased GABA activity --\> sedation, motor dysfunction Decreased Glutamate receptor activity
313
Chronic alcohol use neuroadaptation
Decreased dopamine release and increased receptor expression Decreased GABA receptor expression Increased glutamate release Increased NMDA expression
314
Alcohol and GI tract
Irritant + gastric acid production = gastritis and bleeding Ulcerations Vomiting due to irritation Pancreatitis Upper GI hemorrhage Mallory Weiss tears via vomiting
315
Alcohol and liver
1. Hepatic Steatosis 2. Alcoholic hepatitis 3. Alcoholic cirrhosis
316
Alcohol and hematopoetic system
Anemia - secondary to GI blood loss, vitamin deficienies, bone marrow depression Alcohol induced thrombocytopenia, decreased clotting factor production
317
FAS facial abnormalities
Short palpebral fissures Smooth philtrum Thin upper lip
318
Alcohol and women
Women tend to have higher BAC b/c of no gastric alcohol dehydrogenase and higher body fat --\> smaller volume of distribution Women develop alcohol induced liver disease faster More likely to develop alcoholic hepatitis and die or cirrhosis
319
Alcohol use disorder
Cluster of behavioral and physical symptoms At risk drinkers 3 fold increase in mortality Symptoms include withdrawal, tolerance, craving
320
Drug class for alcohol withdrawal management
Benzos
321
Alcohol and warfarin
Alcohol inhibits CYP450 --\> enhanced warfarin action
322
Alcohol and acetominophen
CYP2E1 induction --\> enhanced production of NAPQI --\> liver toxicity
323
Alcoholic steatosis
Extensive fat accumulation, reversible Microvesicular fat --\> Macrovesicular fat Liver can enlarge
324
Acute alcoholic hepatitis
Liver swollen, edematous, hepatocytes contain Mallory bodies Widespread necrosis and PMNs Pericentral fibrosis Can lead to cirrhosis Hepatocyte injury with balooning degeneration
325
Alcoholic cirrhosis
10-15% of alcoholics Classically micronodular
326
Liver cirrhosis
Parenchymal necrosis Destroyed liver architecture Nodular regeneration often with fobrosis Anorexia, weight loss, ascites, gonadal atrophy, gynecomastia (increased estrogen) Hepatorenal syndrome (severe)
327
Post hepatic causes of Portal HTN
Severe right sided HF Budd Chiari Cosntrictive pericarditis Hepatic veno occlusive disease
328
Intrahepatic causes of portal HTN
Cirrhosis Shistosomiasis Fatty change Sarcoidosis Idiopathic
329
Prehaptic causes of portal HTN
Portal vein thrombosis Splenomegaly AV fistula
330
Biliary stasis
No necrosis Caused by anabolic steroids, progesterone
331
Acute hepatic necrosis causes
Carbon tetrachloride Halothane Paracetamol
332
Chronic parenchymal damage causes
Methyldopa Methotrexate Isoniazid
333
Reyes syndrome
fattty change in liver with encephalopathy Affects children after flu like symptoms Microvesicular steatosis, cerebral edema Biochemical derangement/iral infection affecting mitochondrial metabolism
334
Pre-eclampsia/eclampsia and liver
Small patches of hemorrhage and infarct Hepatic disease is common --\> Hemolysis, elevated liver enzymes, low platelets
335
Acute fatty liver of pregnancy
Wide range disease 3rd trimester Biopsy confirmation Termination of pregnancy