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GIGU Clinical > Week 2 > Flashcards

Week 2 Flashcards

1
Q

If there is an issue in the urea cycle, and the ammonia is not able to be cleared from the body, what could happen?

A

Ammonia could build up in the brain and cause brain damage

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2
Q

What is the committed step of bile acid synthesis?

A

Cholesterol to 7(alpha) hydroxycholesterol with the enzyme 7(alpha) hydroxylase

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3
Q

What does the presence of bile acids do to the synthesis of bile acid?

A

Negative feedback; it inhibits it

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4
Q

What is the function of non-absorbable bile acid binding resins, like cholestyramine?

A

LARGE increase in bile acid excretion

causes a lowering of cholesterol because bile acid synthesis is induced

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5
Q

The induction of _____________ causes the rate of bile acid synthesis to increase

A

7(alpha) hydroxylase

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6
Q

What are gallstones made out of?

A

Bile that is supersaturated with cholesterol

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7
Q

__________ is the insufficient secretion of bile salts or phospholipids into the gall bladder or excess cholesterol secretion into the bile

A

cholelithiasis

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8
Q

What happens in the event of a chronic disturbance in the bile salt mechanisms?

A

malabsorption syndromes and deficiency in fat soluble vitamins

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9
Q

Describe the phases involved in the inactivation and detoxification of xenobiotics

A

Phase 1 increases the polarity and is catalyzed by cytochrome P450 enzymes

Phase 2 takes the primary metabolites to secondary metabolites

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10
Q

Describe a cytochrome P450

Who is her family? 
What is she made of? 
Where does she live? 
Who are her best friends? (what does she co-localize with?) 
How does she work (operate)
A

She’s apart of the CYP superfamily
She has heme containing proteins in her
She is present in the ER
Her bestie is NADPH cytochrome P450 reductase

Use the ETC to get their work done

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11
Q

What do CYPs do?

A

detoxify pharmacological agents

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12
Q

Agents that inhibit CYP will _______ drug levels in plasma

A

increase

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13
Q

Agents that stimulate CYP will cause ______ in drug levels in plasma

A

Decrease

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14
Q

If a patient takes statins with grapefruit juice, what will happen to the statin levels in the plasma?

A

There will be an increase in the statin levels. Citrus juices act as an inhibitor of CYP, which is what allows for the statins to be metabolized. Without the CYP being utilized, statins cannot be broken down which means that they are active in the plasma and they lower the cholesterol that is in the blood too much

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15
Q

If a patient drinks caffeine but is also taking ciprofloxacin, why are their caffeine levels elevated for a longer period of time after consuming the caffeine?

A

The cipro inhibits the CYP1A2 and causes a slower metabolism of the caffeine and causes an increase in the caffeine levels because of the lack of metabolism

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16
Q

Describe personalized medications. How do they work?

A

Everyone has variations of CYPS; so you can genotype for them and treat accordingly

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17
Q

How is tylenol removed from the body?

A

Tylenol conjugates with the glucuronic acid or sulfate and then are excreted via the kidney

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18
Q

Describe what happens in a tylenol overdose

A

Tylenol is conjugated in the kidney by CYP3A4 to NABQ1 which needs to be detoxified by glutathione

If there is a tylenol overdose, the system becomes overwhelmed and the glutathione is not able to detoxify the NABQ1, which is toxic to the liver and causes hepatic failure and death

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19
Q

Why is NABQ1 toxic to the liver?

A

causes free radical mediated per oxidation of membrane lids and damages hepatocytes

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20
Q

A patient comes in with a suspected tylenol overdose, what do you give the patient?

A

N-acetyle cysteine

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21
Q

What are the major changes that occurs with diseases of the liver?

A

Normal leaky membrane that is between endothelial cells is filled with a high density membrane of fibrillar collagen

increased stiffness in the vascular channels leads to portal hypertension

IMPAIRED free exchange of the material between the hepatocytes and blood

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22
Q

What are the labs used to assess liver function on a metabolic panel (list them)

A 
Albumin 
Transaminases 
Alkaline phosphatase 
Prothrombin time (PT) 
Bilirubin 
Urea (BUN)
Glucose 
TAGs 
Cholesterol
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23
Q

If a person has a liver disease, what would you expect the ALT and AST levels to be?

A

ALT And AST levels would be increased because these are released from eh damaged hepatocytes

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24
Q

T/F: ALT is more sensitive because it is cytosolic

A

TRUE

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25
Q

If a person has an issue with Vitamin A storage in the liver, which cells are likely affected?

A

Stellate cells

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26
Q

If someone is dehydrated, what will happen in regards to salivary gland innervation: include mechanistic steps

A

The parasympathetics will be inhibited, Ach will not be released from CN VII and CN IX and is not able to bind to the mCHAR on the acinar and ductal cells

IP3 and CA2+ are NOT increased

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27
Q

What is the effect of ADH And aldosterone on the saliva?

A

Decreases Na composition (absorbs it) and increases K+ concentration (secretes it)

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28
Q

What is the function of HCl

A

initiates protein digestion

pepsinogen to pepsin

kills a large number of bacteria

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29
Q

What is the function of mucus

A

protects the gastric lining from damage by neutralizing acid

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30
Q

What is intrinsic factor?

A

Helps with the absorption of B12

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31
Q

What is released from the parietal cells?

A

Intrinsic factor and HCL

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32
Q

What is released from chief cells?

A

pepsinogen (in response to a low pH)

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33
Q

What is released from G cells

A

Gastrin

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34
Q

What effect does Atropine have on the parasympathetic nervous system?

A

Does not allow the Act to bind to the mACHR

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35
Q

How does omeprazole help to lower the gastric acid in the stomach?

A

IT inhibits the K/H pump that is in the lumen of the parietal cells

Cl does not follow H+ out because H+ isn’t getting out, so there is not any secretion of HCl which will increase the pH in the stomach

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36
Q

As the pH of the gastric acid decreases, what happens to the gastrin release?

A

It is inhibited so that the HCl is not secreted as much

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37
Q

T/F Atropine will block both the direct and indirect pathway of vagal stimulation on the parietal cells

A

False it will only inhibit the direct pathway

Atropine will not have any affect on the gastric secretion

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38
Q

________ acts on G cells to inhibit gastrin release

A

Somatostatin

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39
Q

_________ potentates the actions of ACH and gastrin

A

Histamine

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40
Q

What do antagonists of H2 (cimetidine) receptors do to histamine, Ach, and gastrin?

A

it messes with the H2 receptor and histamine cannot bind, therefore decreasing the abilities of Ach and gastrin

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41
Q

What does an antagonist of an mACHR (atropine) do to histamine, Ach, and gastrin?

A

the effects of ACH will be blocked, which will decreased the Ach-potentiated effects of histamine and gastrin

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42
Q

What is cimetidine used to treat, and why? (MOA)

A

Used to treat duodenal and gastric ulcers as well as GERD because it inhibits the H2 receptors

Normally histamine will cause an increase in gastric function and in turn, an increase in the acidity of the stomach: blocking this will neutralize things and ease the sx

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43
Q

Chewing, swallowing, smell, and test are the stimuli that cause acid secretion during the _______ phase

A

cephalic

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44
Q

Distention of the abdomen will cause the acid secretion during the ________ phase

A

gastric

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45
Q

Digested proteins will cause the acid secretion during the ______ phase

A

intestinal phase

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46
Q

Which phase of gastric acid release will be “abolished” if a vagotomy occurs

A

Cephalic phase

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47
Q

True/False

Coffee (caffeinated and decaf) stimulate gastrin secretion

A

True

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48
Q

_____ _______ stimulation is the most important stimulus for pepsinogen secretion

A

Vagus nerve

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49
Q

True or false: Pepsin does not convert pepsinogen to pepsin, only trypsin can do that

A

False

pepsin do too

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50
Q

Failure to secrete IF is associated with ________ & with absence of parietal cells

A

achlorhydria

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51
Q

If the body does not produce or secrete enough intrinsic factor, what kind of anemia will result and why?

A

Pernicious anemia because of the lack of B12

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52
Q

Atrophic gastritis and autoimmune metaplastic atrophic gastritis are common causes of ________ ________

A

pernicious anemia

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53
Q

What is atrophic gastritis?

A

Inflammation of the stomach mucosa that leads to the loss of parietal cells

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54
Q

What is autoimmune metaplastic atrophic gastritis?

A

The immune system attacks the intrinsic factor protein or gastric parietal cells

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55
Q

What are common causes of an issue with the absorption of vitamin B12

A

Gastrectomy and a gastric bypass

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56
Q

What are the protective factors of gastroduodenal mucosa

A

HCO3 and mucus (protects from the acid)
Prostaglandins
Mucosal blood flow (increased blood flow typically protect)
Growth factors

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57
Q

What are the damaging factors to the gastroduodenal mucosa?

A 
H+ and pepsin 
H pylori 
NSAIDs 
Stress 
Smoking 
Alcohol
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58
Q

In Zollinger Ellison syndrome there is a duodenal or pancreatic neuroendocrine tumor: what does this typically cause?

A

Increased H+ secretion

Increased parietal cell mass

Increased H+ secretory rates

Inhibition of the absorption of sodium and water by the small intestine (secretory diarrhea)

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59
Q

What happens when there is excess H+ in the duodenum?

A

overwhelms the buffer capacity of HCO3 in the pancreatic juice and will create an ulcer

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60
Q

If there is a low pH in the intestinal contents, what will occur physiologically?

A

Inactivates the pancreatic enzymes

Interferes with the emulsification of fat by bile acids

Damages intestinal epithelial cells and villi

Leads to maldigestion and malabsorption

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61
Q

Describe the secretin stimulation test. What is secretin expected to do in a normal person. What is it expected to do with someone who has a gastrinoma?

A

Normal: secretin will cause an inhibition of gastrin release

Gastrinomas: secretin will cause an increase of gastric release

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62
Q

When I say gastrinoma, you say

A

Zollinger Ellison syndrome

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63
Q

Helicobacter pylori and the use of NSAIDS are common causes of ______ ________ _______

A

peptic ulcer disease (ulcers)

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64
Q

If there is a loss of the protective mucosal barrier or an increase in H+ and pepsin secretions or a combination of the two (from NSAIDs, or bacteria), what is a common outcome of this?

A

Peptic ulcer disease

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65
Q

There are two common types of peptic ulcer disease disease

A

Gastric ulcers

Duodenal ulcers

66
Q

_________ releases cytotoxins that breakdown the mucosal barrier and underlying cells

A

H. Pylori

67
Q

The enzyme ______ allows the bacteria to colonize the gastric mucosa in an H. pylori infection. How dies this enzyme work? ie what is the mechanism of action?

A

urease

Urease converts the urea to ammonia to alkalize the environment creating ammonium which is cytotoxic

68
Q

What does ammonium do to the cell?

A

Damages the epithelial cells and breaks the mucosal barrier

69
Q

how is H. pylori diagnosed?

A

By administering a test of urease activity

70
Q

______ _______ form on the lining of the stomach and occur because there is a defect in the gastric mucosal barrier

A

Gastric ulcers

71
Q

_____ _______ form on the lining of the duodenum; are the most common, an do not become malignant: H+ secretion rates are increased

A

Duodenal ulcers

72
Q

In cystic fibrosis, the _____ is one of the first organs to fail

A

pancreas

Cl is not able to get out of the cell and be cotransported with HCO3

73
Q

The phases of the pancreas are the same as the stomach: cephalic, gastric, and intestinal: which two produce only enzymatic secretions, and which one secretes enzymatic and aqueous secretions?

A

Cephalic and gastric only secrete enzymatic

Intestinal secretes aqueous and enzymatic

74
Q

How is C-peptide used as a diagnostic tool for diabetes?

A

C-peptide is secreted when proinsulin is cleaved into insulin, if there are low levels of c-peptide, then you can assume that the patient has type 1 diabetes

75
Q

What would you expect the c-peptide levels to be in type 2 diabetes?

A

Since the insulin is able to get out, but it is an issue in the receptor causing the pathology, then you would expect the insulin to be higher because it is not able to reach the receptor

C-peptide has a higher half life than insulin

76
Q

Type 1 or Type 2 DM?

Destruction of B cells

A

Type 1

77
Q

Type 1 or Type 2 DM?

Insulin resistance

A

Type 2

78
Q

Type 1 or Type 2 DM?

K+ goes out of the cells and there is a lack of insulin effect on the Na/K ATPase

A

Type 1 DM

79
Q

Type 1 or Type 2 DM?

A patient comes in with an increased blood glucose, increased blood amino acid concentration, polyuria, polydipsia

A

Type 1

80
Q

Type 1 or Type 2 DM?

A patient comes in with hyperkalemia?

A

Type 1 DM

the body secretes potassium in order to try to get insulin to be released, because potassium is a stimulating factor

81
Q

What will happen to blood sugar levels during exercise?

A

Blood sugar will decrease because AMPK is activated and GLUT4 is taken to the membrane so that glucose is able to supply the muscles

82
Q

What effect does fasting have on insulin and glucagon?

A

Inhibits insulin release

Stimulates glucagon release

83
Q

Describe incretin

A

Intestinal derived hormone that is secreted in response to GI glucose and fat

stimulates insulin secretion and inhibits glucagon secretion; slowing gastric emptying

84
Q

Describe what happens to the muscular system when there is an insulin deficiency or an insulin resistance

A

There is a decreased tissue glucose utilization which leads to increased amino acid catabolism

There will be an increased blood level of amino acids in the blood in t1DM

These are then able to go to the liver and aid gluconeogeneis which leads to hyperglycemia, which causes the kidney to excrete more urine, resulting in a urine depletion which then causes polydipsia

85
Q

Describe what happens to adipose tissue when there is an insulin deficiency or resistance

A

There is increased lipolysis which leads to polyphagia, and ketogenesis in the liver

This can lead to an increase in ketoacidosis causing a diabetic coma or causing the kidney to release more urine, resulting in volume depletion and polydipsia

86
Q

If there is a decreased GLUT 4 uptake, decreased ability of insulin to repress hepatic glucose production, and the inability of insulin to repress adipose tissue uptake and lipolysis, which is likely being described?

A

Obesity induced insulin resistance

87
Q

Autoimmune thyroid disease, celiac disease, and addisons disease are all associated conditions of _______

A

T1DM

88
Q

Obesity, lipid abnormalities, PCOS and NAFLD are associated conditions of ______

A

T2DM

89
Q

Why is IgA commonly used by the GI system immunologically?

A

does NOT activate complement

does not activate phagocytes

resistant to proteolysis by the peptidases in the stomach, small intestine, and the pancreas

90
Q

Undigested dietary carbohydrates produce_____

A

SCFAs: acetate, propionate, and butyrate

91
Q

Differentiate between a non-immune mediated and an immune-mediated reaction

A

non-mediated is more of a food intolerance

immune mediated is a food allergy

92
Q

________ _______ _______ is a chronic condition that can cause cramping, constipation, and diarrhea

A

IBS

93
Q

_______ ________ is caused by toxins such as bacteria in spoiled food can cause severe digestive symptoms.

A

food poisoning

94
Q

______ _______ is a chronic digestive condition that is triggered by eating gluten

A

Celiac disease

95
Q

Describe an IgE food allergy in terms of

1. first exposure

A

The allergen is ingested

B cells interact with the allergen and create a plasma cell that releases IgE to the mast cells

IgE binds to the mast cell

96
Q

Describe an IgE food allergy in terms of

2. Second exposure

A

Allergen is ingested

cross links to the mast cell in the tissues

releases vasoactive amines, cytokines, and lipids

97
Q

What is the role of Treg cells in control of food allergies?

A

To inhibit the mast cell reactivity, reduce IgE synthesis, and increase IgG and IgA synthesis

Also inhibit Th1, Th2, and Th17 cells from creating an inflammatory response

98
Q

Vitamin D, Vitamin A, and folate ______ inflammatory responses

A

suppress

99
Q

Describe the non-IgE mediated allergic reaction to peanuts

A

Peanuts can cause a production of C3a

c3A will stimulate the macrophages, basophils, and mast cells

PAF and histamine increases the vascular permeability and smooth muscle contractility

100
Q

If a patient ingests a peanut and there is an increase in the amount of IgG1 that is present in the cell, what will likely happen after that?

A

There will be an increase in allergen-Ab complexes and macrophage activation that will release PAF

101
Q

The ______ and _______ are molecules that are a predisposing factor for celiac disease

A

HLA-DQ2 and HLA-DQ8

immune response against gluten peptides

102
Q

A patient with celiac disease, typically has serum antibodies against an enzyme, _____ _________ ___

A

Tissue transglutaminase 2`

103
Q

This proline rich protein is poorly digested in the small intestinal tract and is rich inglutamine resides

A

Gluten

104
Q

Describe what happens when a person with celiac disease is exposed to gluten

A

The antibodies that the patient has to TG2 will not allow the gluten to be broken down into glutamate and broken down. Instead it will cause an inflammatory T cell mediated response against the bowels leading to malabsorption

105
Q

What is the preferred screening method of celiac disease?

A

tTG-IgA test

106
Q

What ethnic groups are most at risk of developing T2DM?

A

African americans
Native americans
Hispanic

107
Q

Which genes are involved in T1DM

A

HLADQ2 and DQ8

108
Q

_____ expression and presentation of insulin in thymus to developing T cells in critical to protecting against development of T1DM.

A

AIRE

109
Q

True/False: Decreased breast feeding does not have an effect on T1DM

A

False

Decreased breast feeding is linked to diabetes because cows milk has less insulin, so the baby isn’t getting as much exposure

110
Q 
A patient comes in and has increased 
M1 macrophages 
mast cells 
B2 cells 
CD8 T cells 
IFNy and Th1 
in the tissues, would you expect them to have T1DM or T2DM?
A

T2DM: inflammatory processes in the adipose tissues is a common sign of obese adipocytes, which are associated with T2DM

111
Q

True/False: The presences of 2+ antibodies is highly predictive of future T1DM

A

True

112
Q

_______ is when liver cells are damaged and replaced by scar tissue. Excessive alcohol intake is a common cause

A

Cirrhosis

113
Q

______ _______ can be caused by cirrhosis

A

Portal hypertension

114
Q

______ ______ are swollen connection between systemic and portal systems at inferior end of esophagus

A

Esophageal varices

115
Q

______ _____ swollen connections between systemic and portal systems around umbilicus

A

Caput medusae

116
Q

If there are elevated aminotransferases, there is likely what pathology present?

A

Hepatocyte injury; liver injury

117
Q

If there is an elevation in the alkaline phosphate of the serum, what is likely the pathology that is present?

A

Bile duct injury- cholestasis

118
Q

________ measures the livers ability to detoxify metabolites and transport organic anions into the bile

A

Bilirubin

119
Q

When the function of the liver declines, what will happen to the level of albumin?

A

It will decline as well. Albumin is made in the liver

120
Q

What does prothrombin show?

A

Reflects the degree of hepatic synthetic dysfunction

it increases as the ability of a cirrhotic liver to synthesize clotting factor diminishes

121
Q

_______ _______ is caused by increased conjugated bilirubin in the first week of postnatal and is caused by the breakdown of erythrocytes and low activity of UDP glucuronyl transferase

A

Physiological jaundice

122
Q

What kind of bilirubin is produced in hemolytic anemia?

A

Increased unconjugated bilirubin

123
Q

This is a defect in the ability of the hepatocytes to secrete conjugated bilirubin into the bile

A

Dubin-Johnson syndrome

124
Q

What is mutated in Dubin-Johnson syndrome?

A

MRP2

125
Q

What are some of the sx of Dubin Johnson syndrome?

A

Mild jaundice throughout life that is worsened by alcohol, BCPs, infection, and pregnancy

BLACK liver

126
Q

Describe Gilberts disease

A

Mutation in the gene that codes for UDP glucuronyltransferase

causes hyperbilirubinemia when stressed

increased unconjugated bilirubin in the blood

127
Q

_____ _______ syndrome is the mutation in the gene that codes for UDP glucuronyltransferase and can occur in two types

A

Crigler Najjar syndrome

128
Q

Describe type 1 Crigler Najjar syndrome

A

noticed early in life

UDP glucuronyltransferase is not functional

characterized by CP, Sensorineural hearing loss, and eye gaze issues

damages neurons, astrocytes, and microglia (kernicterus)

129
Q

Describe type 2 Crigler-Najjar syndrome

A

Diagnosed later in life, less function of the UDP glucuronlytransferase

survive

130
Q

List the treatments that are sometimes used in Crigler-Najjar syndrome

A 
Phototherapy: bilirubin lights 
Blood transfusions 
Oral calcium phosphate and carbonate 
Liver transplant 
phenobarbital
131
Q

_____ ______ is the buildup of conjugated and unconjugated bilirubin due to mutations in OATP1B1

A

Rotor syndrome

132
Q

What does OATP1B1 do?

A

transports bilirubin and other components from the blood to the liver

133
Q

________ are caused by too much absorption of water from bile, too much absorption of bile acids from bile, too much cholesterol in bile, inflammation of the epithelium

A

Gall stones

134
Q

Where do most of the gallstones form?

A

In the body of the gallbladder; usually asymptomatic

135
Q

_______ is the inflammation of the gallbladder from obstruction of the cystic duct from a stone

A

Cholecystitis

136
Q

Gallstones that are occluding the common bile duct are called __________

A

choledocholithiasis

jaundice and conjugated hyperbilirubinemia

137
Q

______ is the infection of the bile duct

A

Cholangitis

138
Q

What are the symptoms that are seen with a leptin or a leptin receptor gene deficiency?

A

Early onset severe obesity, infertility, hyrerphagia, infections

139
Q

What are the symptoms of melanocortin 4 receptor gene mutation

A

Early onset severe obesity, increased linear growth, hyrerphagia, hyperinsulinemia

140
Q

What are the symptoms of Prader will syndrome?

A

Neonatal hypotonia, slow infant growth, small hands and feet, mental retardation, hypogonadism, hyrerphagia, leading to severe obesity, elevated gherkin

141
Q

What are the symptoms of a POMC deficiency

A

obesity, red hard, adrenal insufficiency due to ACTH, hyperproinsulinemia, hyrerphagia, pale skin, cholestatic jaundice

142
Q

If the vagal activity is blocked, then the amount of material that is in the stomach no longer influences _____ ______

A

meal size

143
Q

What is the lateral hypothalamic area involved in?

A

It is the hunger center

144
Q

The satiety center is the ______ _______ ______

A

ventromedial hypothalamic nucleus

145
Q

What stimulates the orexigenic pathway?

A

hunger, and it makes you want to eat more

146
Q

What are the orexigenic hormones?

A

Ghrelin

147
Q

What is the anorexigenic pathway hormones?

A

Insulin
CCK
PPY
Leptin

148
Q

______ is secreted in the stomach by endocrine cells, bind to growth hormone receptors and stimulate the neurons that release NPY

A

Ghrelin

149
Q

What are the actions of Ghrelin?

A 
Increased appetite 
Increased gastric motility 
Increased gastric acid secretion 
Increased adipogenesis 
Decreased insulin secretion
150
Q

______ binds to receptors in the POMC And the NPY systems to inhibit NPY and stimulate POMC

A

Insulin

151
Q

What are the actions of insulin?

A

Increased appetite

Increased metabolism

152
Q

______ is released by I cells in the duodenum and allows for satiety

A

CCK

153
Q

_____ is released by the L cells of the ileum and binds to Y2R in the hypothalamus to inhibit NPY and stimulate (released inhibition) of POMC

A

PYY

154
Q

Leptin is secreted by _____ cells and inhibits the NPY system and stimulates the POMC system

A

adipose

155
Q

What does the appetite suppressing hormone do?

A

Decreases appetite, increases metabolism, and decreases gherkin release

156
Q

Describe glucagon like peptide GLP1

A

proglucagon derived peptide

secreted with PYY From L cells in the ileum

incretin

levels will rise after a meal and fall during fasting

reduces food intake, suppresses glucagon secretion, and delays gastric emptying

157
Q

________ is released from the L cells in response to ingested food in proportion of the caloric intake

A

Oxyntomodulin

158
Q

_______ _______ is secreted from the islet of Langerhans, it decreases the food intake through the Y4R in the brainstem and hypothalamus

A

Pancreatic peptide

159
Q

Anorexia nervosa causes several hormonal changes. List some of these

A

Polymorphisms in the genes that are involved in eating attitudes, regulation of eating behavior and reward mechanisms

Leptin is released

Ghrelin becomes resistant

PYY is elevated

160
Q

What two genes help with protection from T1DM?

A

DR2 and DQ6

GIGU Clinical (5 decks)

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