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Pathophys > Endo Patho > Flashcards

Endo Patho Flashcards

1
Q

What is the exocrine role of the pancreas

A

Secretes digestive enzymes into duodenum

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2
Q

what is the endocrine role of the pancreas

A

secretes insulin(60%), glucagon(25%), and somatostatin(10%) into the blood from pancreatic islet cells

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3
Q

what are pancreatic Acinar cells and what do they secrete?

A

exocrine cells that secrete pancreatic enzymes
Amylase: carb breakdown
Lipase: lipid breakdown
DNA-ase: nucleic acid breakdown
RNA-ase: nucleic acid breakdown
Zymogens: Trypsinogen Chymotrypsinogen, Procarboxypeptidase A, B

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4
Q

what is the role of zymogens

A

enzymes that have no activity until they are cleaved (won’t destroy the pancreas)

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5
Q

how is insulin affected by dec liver function

A

insulin is degraded by insulinase which is produced in the liver. dec liver function=inc insulin half life

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6
Q

what is proinsulin

A

=insulin+C-peptide. It is the storage form of insulin. 5-10% of secreted product is in proinsulin form.

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7
Q

what is the half lives of C-peptide and insulin and how does this affect lab results

A

C-Peptide= hours
insulin= 6min
Check C-peptide levels to see if insulin is being released bc insulin doesn’t last as long.

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8
Q

how does insulin affect glucose, FFA, and AA

A

storage hormone changing glucose to glycogen, FFA to Triglycerides, and AA to proteins. It inhibits the reverse process. This causes cell growth and differentiation.

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9
Q

what is GLUT4

A

GLUT4 is the insulin-regulated glucose transporter found in adipose tissues and striated muscle

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10
Q

what is GLUT1. What is the effect from blocking it?

A

Glu transporter in GI and kidneys. Doesn’t require insulin to absorb glu.
Blocking= dec blood glu but causes diarrhea

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11
Q

what is GLUT2? What is the effect from blocking it?

A

found in prox segment in kidney. Also doesn’t require insulin to reabsorb glu from urine(up to 180).
Blocking= dec blood glu without GI SE

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12
Q

what is the pathway of Glu causing insulin release in B cells

A

GLUT2 transports Glu into B cells= mitochondria produces ATP= inhib sulfonylurea receptor(K+ channel)=cell membrane depolarization= opens Ca channel= Ca influx= stimulates Ca dependent insulin release

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13
Q

how do sulfonylurea drugs work

A

block K+ channel= inc insulin release

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14
Q

what is glycogenesis

A

glu to glycongen

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15
Q

what is insulins effect in muscle tissue

A 
Increases glucose and amino acid uptake
Stimulates
Glycogenesis: glucose  to glycogen
Lipogenesis: glucose to triacylglycerol
Protein synthesis: amino acids to protein

Inhibits
Gluconeogenesis: protein/lipids to glucose
Glycogenolysis: glycogen to glucose
Ketogenesis(lipolysis): lipids to ketones
Proteolysis: proteins to amino acids

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16
Q

what is insulins effect in the hepatic tissue

A 
Increases glucose uptake
Stimulates
Glycogenesis: glucose  to glycogen
Lipogenesis: glucose to triacylglycerol
Protein synthesis: amino acids to protein

Inhibits
Gluconeogenesis: protein/lipids to glucose
Glycogenolysis: glycogen to glucose
Ketogenesis(lipolysis): lipids to ketones

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17
Q

what is insulins effect in adipose tissue

A 
Increases glucose uptake
Stimulates
Lipogenesis: glucose to triacylglycerol
Inhibits
Ketogenesis(lipolysis): lipids to ketones
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18
Q

what plasma glu level stimulates insulin release

A

> 80

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19
Q

at what plasma glu level is max insulin release

A

> 200

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20
Q

what inhibits insulin secretion

A

fasting, exercise, sympathetic activity/Alpha adrenergic stimulation(norepi, epi)

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21
Q

what stimulates insulin secretion

A

Glu, AA, FFA, gastro-intestinal hormones, neural influence

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22
Q

what gastro-intestinal hormones stimulate insulin secretion

A

Glucagon-like peptide 1 (GLP-1)
Gastric inhibitory polypeptide (GIP)
Secretin

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23
Q

what neural influences stimulate insulin secretion

A

PNS Stimulation

SNS via beta adrenergic(alpha cells predominate)

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24
Q

what problems might B-blockers cause in DM

A

beta adrenergic nerves stimulate insulin release. Blocking this can inc blood glu

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25
Q

what is glucagon’s effect

A

opposite of insulin

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26
Q

what stimulates glucagon secretion

A

hypoglycemia, AAs, Fasting, exercise, sympathetic B-adrenergic stimulation(norepi, epi)

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27
Q

what inhibits glucagon effects

A

glucose, insulin, FFAs, alpha-adrenergic stimulation

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28
Q

why does inc sympathetic B-adrenergic stimulation cause secretion of both insulin and glucagon?

A

need glucagon to inc blood glu and need insulin to inc metabolism

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29
Q

why does AAs cause secretion of both insulin and glucagon?

A

it allows for protein synthesis to occur while maintaining blood glu levels after high protein and low carb meals

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30
Q

what are normal, impaired glucose tolerance, and DM ranges for fasting plasma glu

A

normal 125

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31
Q

what are normal, impaired glucose tolerance, and DM ranges for oral glu test post 2hrs

A

normal 200

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32
Q

what are normal, impaired glucose tolerance, and DM ranges for A1C

A

normal 6.5%

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33
Q

what is the genetic component of DM1

A

95% of Caucasians have HLA-DR3 or HLA-DR4 with 40% having both
Insulin gene with variable number of tandem repeats in promoter
Monozygotic twins: 30%-50% Concordance

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34
Q

what is the genetic component of DM2

A

Genetic, but diff. from Type 1
>1/3rd have at least 1 parent with Type 2
Monozygotic twins: 100% concordance for Type 2 DM
Inheritance patter complex: multiple interacting susceptibility genes.

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35
Q

what is the autoimmune component of DM1

A

Post viral infection: mumps, rubella, coxsackieB, cytomegalovirus
T –cell response
Antibodies to beta cells

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36
Q

what is the autoimmune component of DM2

A

There is no autoimmune component to DM2

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37
Q

what is Maturity Onset diabetes of the young (MODY)

A

young pts develop DM2 from Mutations in a variety of genes (not from obesity) especially glucokinase mutation
primary beta cell defects

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38
Q

what is Maternally inherited diabetes and deafness caused from

A

microsomal DNA mutations

39
Q

what causes gestational DM

A

either too much or increased sensitivity to human placental lactogen which is a protein in the mother that casues a rise in BS

40
Q

when/how do you test for gestational DM

A

oral glu challenge test in 3rd semester

41
Q

what is the rule of 1/3s with gestational DM

A

1/3 keep DM2 post delivery
1/3 have inc risk of DM2 post delivery
1/3 do not have inc risk of DM2 post delivery

42
Q

what are the components of metabolic syndrome

A 
Obesity (abdominal)
Insulin resistance
Fasting Hyperglycemia
Increased lipids
Hypertension
43
Q

what is the pathogenesis of DM1

A

T-Lymphocytes reacting against poorly defined beta cell antigens

Inflammatory infiltrate, chronic, i.e., “INSULITIS”

44
Q

what is the pathogenesis of DM2

A

INSULIN RESISTANCE
Beta cells UN-able to adapt to the “long term demands of insulin resistance”
Accumulation of amyloid protein

45
Q

what is insulitits

A

inflammation of the islets of Langerhans of the pancreas

46
Q

how does amyloidosis affect the pancreas

A

destroys the pancreatic islet in DM2

47
Q

what % of beta cells are destroyed before manifestation of DM1 Sx

A

90%

48
Q

how does DM inc risk for infection

A

Due to:
Impaired senses

Tissue hypoxia

Pathogens proliferate well in glucose

Decreased delivery of WBC’s

Altered WBC function

49
Q

where are common infection locations due to DM

A 
SKIN
Lungs
-TUBERCULOSIS
-PNEUMONIA
Kidneys
-PYELONEPHRITIS
Multiple locations
-CANDIDA
50
Q

what are the most common islet cell tumors? What others can occur?

A

Beta cells INSULINOMAS (NOT rare)
Alpha cells GLUCAGONOMAS (rare)
Delta cells SOMATOSTATINOMAS (rare)

51
Q

what are gastrinomas

A

a gastrin-secreting tumor that can occur in the pancreas, although it is most commonly found in the duodenum. They produce ZOLLINGER-ELLISON SYNDROME, consisting of increased acid and ulcers

52
Q

what are acute complications of DM

A

Hypoglycemia
Diabetic ketoacidosis (DKA)
Hyperosmolar Hyperglycemic NonKetotic Coma (HHNKC)

53
Q

what are chronic complications of DM

A 
Macrovascular Disease:  atherosclerosis
-CAD
-CVA
Microvascular Disease
-Kidney:  nephropathy
-Retina:  retinopathy 
-Nerves:  neuropathy
Immune
-infections
54
Q

what are hypoglycemic levels in newborns and adults? Why are newborns lower?

A

adults=<35

Newborns can use other sources besides glu for energy in the brain

55
Q

what can cause hypoglycemia

A

Too much insulin
Decrease caloric intake
Exercise
Medications

56
Q

what medication has a high risk of hypoglycemia

A

Sulfonylurea- may cause too much insulin to be released

57
Q

how does hypoglycemia affect the nervous system

A

mainly affects the SNS

  • tachy
  • diaphoresis
  • tremors
  • pallor
  • anxiety
58
Q

what are the cellular manifestations of hypoglycemia

A
  • HA
  • dizziness
  • irritability
  • fatigue
  • confusion
  • visual changes
  • hunger
  • Sz
  • coma
59
Q

what is AKDA?

A

increase blood glucose with hormonal shift to antagonize insulin
9% mortality

60
Q

what is the most common precipitating factor of DKA and how does it elevate BS?

A

illness/stress=inc cortisol= inc insulin resistance=inc glucagon and cortisol production= mobilize stored nutrients= further inc BS

61
Q

what causes a well controlled DM1 to get DKA

A

inc cortisol= inc insulin resistance

62
Q

what BS levels correspond to trace and 1+ urine dipstick glu levels

A

trace=100mg/dl

1+= 250mg/dl

63
Q

how does inc release of glucagon, epi, GH, cortisol in DKA lead to coma

A

1) =inc FFA in blood= ketone body formation= metabolic acidosis= CNS depressant
2) =inc glycogenolysis=hyperglycemia= glycosuria= polyuria= dehydration= hyperosmolarity= CNS depressant

64
Q

at what BS levels can DKA induce coma in DM1

A

300-400 due to acidity and osmolarity changes

65
Q

at what BS levels can DKA induce coma in DM2

A

600-800 due to osmolarity changes

66
Q

why is IV insulin given in DKA

A

dehydration would dec absorption of subq insulin

67
Q

why is K+ falsely elevated in DKA

A

During DKA, there is inc H+ uptake into RBC by kicking out K+ creating false elevated K+ in serum. As you tx acidity, K+ will return into the RBC. Also insulin causes K+ to go into cells independent of H/K pump

68
Q

What are the 3 main focuses of DKA tx?

A

fluids, K+, and insulin

69
Q

How are fluids used in DKA tx

A

1) always start with NS (to prevent neuro swelling=diabetic neuropathy).
2) Then check the corrected Na. If >135 give .45NS, if <200 give fluid with dextrose to prevent delayed insulin effect.

70
Q

what type of pt do fluids need to be given cautiously to?

A

Cardiac Dz pts

71
Q

What insulin dose is used for DKA tx?

A

0.1U/kg IV

72
Q

what are the characteristics of HHNKC

A

Low levels of FFA, therefore, no ketones

Sufficient insulin:

Extremely high glucose levels & severe volume loss and dehydration.

73
Q

what is the Tx for HHNKC

A

fluid replacement, K+, and insulin

74
Q

what is the somogyi effect

A

seen in DM1
Nocturnal hypoglycemia: increase insulin sensitivity

Rebound hyperglycemia

Manifestations: nightmares and morning headaches

75
Q

how does the dawn effect differ from somogyi effect

A

Also in DM1, but no hypoglycemia at night

76
Q

what is the somogyi effect tx?

A

protein rich diet prior to bedtime

77
Q

what is the protein glycation pathway in chronic DM

A

induced by chronic DM
Non-enzymatic glycosylation
Occurs in proportion to the severity of hyperglycemia
Advanced glycosylation consists of covalently bound glucose: leads to physical cross-linking of nearby proteins contributing to thickening of vascular basement membranes.

78
Q

what is the aldose redcutase pathway in chronic DM

A

Glu enters cells and is converted to Sorbitol production

Binds to basement membrane around vessels and nerves

79
Q

what is the protein kinase C activation pathway in chronic DM

A

Increased production of extracellular matrix and cytokines
Enhanced microvascular contractility & permeability
Proliferation of endothelial and smooth muscle cells

80
Q

how does chronic DM cause macrovascular dz

A

glu sticks on inside of vessles which makes it easier for fats to stick and form plaques causing atherosclerosis.

81
Q

how does improvement in A1C levels affect macrovascular outcomes in DM2

A

studies have shown it has not been effective

82
Q

what signs of retinopathy are associated with chronic DM

A 
Microaneurysms
Areas of hemorrhage
Cotton wool spots
Hard exudates
Venous beading
Neovascularization
Retinal detachment
Vitreous detachment
Pre retinal hemorrhage
83
Q

what is the first stage of DM retinopathy

A

Nonproliferative retinopathy
Increased retinal capillary permeability, vein dilation, microaneurysm formation and superficial and deep hemorrhages

84
Q

what is the second stage of DM retinopathy

A

Preproliferative retinopathy

Progressive retinal ischemia with areas of poor perfusion resulting in infarctions

85
Q

what is the third stage of DM retinopathy

A

Proliferative retinopathy
Presence of neovascularization and fibrous tissue formation within the retinal or optic disc
May see retinal detachment or hemorrhage into the vitreous humor

86
Q

how can DM cause serious visual loss

A

formation of exudates, edema or ischemia occurs nears the fovea.

87
Q

what is renal hyaline arteriolosclerosis?

A

marked thickened afferent arteriole

88
Q

what effect does chronic DM have on the kidneys

A

1-thickened glomerular basement membrane
2-thinning of cortical tissue
3-diffuse granular surface of kidneys

89
Q

what are Kimmelstiel-Wilson(KW) Kidneys

A

nodular glomerulosclerosis from DM damage

90
Q

what is the metabolic theory of DM neuropathy

A

neuropathy caused from production of sorbitol

91
Q

what is the vascular theory of DM neuropathy

A

neuropathy caused from dec blood flow

92
Q

what is the subclinical stage of DM neuropathy

A

slowed motor & sensory nerve conduction without manifestations

93
Q

what is the clinical stage of DM neuropathy

A

Symptoms present

Sensory before motor, distal degeneration, unmyelinated neurons affected first

94
Q

what effect does DM neuropathy have on the autonomics

A

dec GI motility

postural hypotension

Pathophys (15 decks)

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