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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
what is glucagon's effect
opposite of insulin
26
what stimulates glucagon secretion
hypoglycemia, AAs, Fasting, exercise, sympathetic B-adrenergic stimulation(norepi, epi)
27
what inhibits glucagon effects
glucose, insulin, FFAs, alpha-adrenergic stimulation
28
why does inc sympathetic B-adrenergic stimulation cause secretion of both insulin and glucagon?
need glucagon to inc blood glu and need insulin to inc metabolism
29
why does AAs cause secretion of both insulin and glucagon?
it allows for protein synthesis to occur while maintaining blood glu levels after high protein and low carb meals
30
what are normal, impaired glucose tolerance, and DM ranges for fasting plasma glu
normal 125
31
what are normal, impaired glucose tolerance, and DM ranges for oral glu test post 2hrs
normal 200
32
what are normal, impaired glucose tolerance, and DM ranges for A1C
normal 6.5%
33
what is the genetic component of DM1
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
34
what is the genetic component of DM2
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.
35
what is the autoimmune component of DM1
Post viral infection: mumps, rubella, coxsackieB, cytomegalovirus T –cell response Antibodies to beta cells
36
what is the autoimmune component of DM2
There is no autoimmune component to DM2
37
what is Maturity Onset diabetes of the young (MODY)
young pts develop DM2 from Mutations in a variety of genes (not from obesity) especially glucokinase mutation primary beta cell defects
38
what is Maternally inherited diabetes and deafness caused from
microsomal DNA mutations
39
what causes gestational DM
either too much or increased sensitivity to human placental lactogen which is a protein in the mother that casues a rise in BS
40
when/how do you test for gestational DM
oral glu challenge test in 3rd semester
41
what is the rule of 1/3s with gestational DM
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
what are the components of metabolic syndrome
``` Obesity (abdominal) Insulin resistance Fasting Hyperglycemia Increased lipids Hypertension ```
43
what is the pathogenesis of DM1
T-Lymphocytes reacting against poorly defined beta cell antigens Inflammatory infiltrate, chronic, i.e., “INSULITIS”
44
what is the pathogenesis of DM2
INSULIN RESISTANCE Beta cells UN-able to adapt to the “long term demands of insulin resistance” Accumulation of amyloid protein
45
what is insulitits
inflammation of the islets of Langerhans of the pancreas
46
how does amyloidosis affect the pancreas
destroys the pancreatic islet in DM2
47
what % of beta cells are destroyed before manifestation of DM1 Sx
90%
48
how does DM inc risk for infection
Due to: Impaired senses Tissue hypoxia Pathogens proliferate well in glucose Decreased delivery of WBC’s Altered WBC function
49
where are common infection locations due to DM
``` SKIN Lungs -TUBERCULOSIS -PNEUMONIA Kidneys -PYELONEPHRITIS Multiple locations -CANDIDA ```
50
what are the most common islet cell tumors? What others can occur?
Beta cells INSULINOMAS (NOT rare) Alpha cells GLUCAGONOMAS (rare) Delta cells SOMATOSTATINOMAS (rare)
51
what are gastrinomas
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
what are acute complications of DM
Hypoglycemia Diabetic ketoacidosis (DKA) Hyperosmolar Hyperglycemic NonKetotic Coma (HHNKC)
53
what are chronic complications of DM
``` Macrovascular Disease: atherosclerosis -CAD -CVA Microvascular Disease -Kidney: nephropathy -Retina: retinopathy -Nerves: neuropathy Immune -infections ```
54
what are hypoglycemic levels in newborns and adults? Why are newborns lower?
adults=<35 | Newborns can use other sources besides glu for energy in the brain
55
what can cause hypoglycemia
Too much insulin Decrease caloric intake Exercise Medications
56
what medication has a high risk of hypoglycemia
Sulfonylurea- may cause too much insulin to be released
57
how does hypoglycemia affect the nervous system
mainly affects the SNS - tachy - diaphoresis - tremors - pallor - anxiety
58
what are the cellular manifestations of hypoglycemia
- HA - dizziness - irritability - fatigue - confusion - visual changes - hunger - Sz - coma
59
what is AKDA?
increase blood glucose with hormonal shift to antagonize insulin 9% mortality
60
what is the most common precipitating factor of DKA and how does it elevate BS?
illness/stress=inc cortisol= inc insulin resistance=inc glucagon and cortisol production= mobilize stored nutrients= further inc BS
61
what causes a well controlled DM1 to get DKA
inc cortisol= inc insulin resistance
62
what BS levels correspond to trace and 1+ urine dipstick glu levels
trace=100mg/dl | 1+= 250mg/dl
63
how does inc release of glucagon, epi, GH, cortisol in DKA lead to coma
1) =inc FFA in blood= ketone body formation= metabolic acidosis= CNS depressant 2) =inc glycogenolysis=hyperglycemia= glycosuria= polyuria= dehydration= hyperosmolarity= CNS depressant
64
at what BS levels can DKA induce coma in DM1
300-400 due to acidity and osmolarity changes
65
at what BS levels can DKA induce coma in DM2
600-800 due to osmolarity changes
66
why is IV insulin given in DKA
dehydration would dec absorption of subq insulin
67
why is K+ falsely elevated in DKA
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
What are the 3 main focuses of DKA tx?
fluids, K+, and insulin
69
How are fluids used in DKA tx
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
what type of pt do fluids need to be given cautiously to?
Cardiac Dz pts
71
What insulin dose is used for DKA tx?
0.1U/kg IV
72
what are the characteristics of HHNKC
Low levels of FFA, therefore, no ketones Sufficient insulin: Extremely high glucose levels & severe volume loss and dehydration.
73
what is the Tx for HHNKC
fluid replacement, K+, and insulin
74
what is the somogyi effect
seen in DM1 Nocturnal hypoglycemia: increase insulin sensitivity Rebound hyperglycemia Manifestations: nightmares and morning headaches
75
how does the dawn effect differ from somogyi effect
Also in DM1, but no hypoglycemia at night
76
what is the somogyi effect tx?
protein rich diet prior to bedtime
77
what is the protein glycation pathway in chronic DM
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
what is the aldose redcutase pathway in chronic DM
Glu enters cells and is converted to Sorbitol production | Binds to basement membrane around vessels and nerves
79
what is the protein kinase C activation pathway in chronic DM
Increased production of extracellular matrix and cytokines Enhanced microvascular contractility & permeability Proliferation of endothelial and smooth muscle cells
80
how does chronic DM cause macrovascular dz
glu sticks on inside of vessles which makes it easier for fats to stick and form plaques causing atherosclerosis.
81
how does improvement in A1C levels affect macrovascular outcomes in DM2
studies have shown it has not been effective
82
what signs of retinopathy are associated with chronic DM
``` Microaneurysms Areas of hemorrhage Cotton wool spots Hard exudates Venous beading Neovascularization Retinal detachment Vitreous detachment Pre retinal hemorrhage ```
83
what is the first stage of DM retinopathy
Nonproliferative retinopathy Increased retinal capillary permeability, vein dilation, microaneurysm formation and superficial and deep hemorrhages
84
what is the second stage of DM retinopathy
Preproliferative retinopathy | Progressive retinal ischemia with areas of poor perfusion resulting in infarctions
85
what is the third stage of DM retinopathy
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
how can DM cause serious visual loss
formation of exudates, edema or ischemia occurs nears the fovea.
87
what is renal hyaline arteriolosclerosis?
marked thickened afferent arteriole
88
what effect does chronic DM have on the kidneys
1-thickened glomerular basement membrane 2-thinning of cortical tissue 3-diffuse granular surface of kidneys
89
what are Kimmelstiel-Wilson(KW) Kidneys
nodular glomerulosclerosis from DM damage
90
what is the metabolic theory of DM neuropathy
neuropathy caused from production of sorbitol
91
what is the vascular theory of DM neuropathy
neuropathy caused from dec blood flow
92
what is the subclinical stage of DM neuropathy
slowed motor & sensory nerve conduction without manifestations
93
what is the clinical stage of DM neuropathy
Symptoms present | Sensory before motor, distal degeneration, unmyelinated neurons affected first
94
what effect does DM neuropathy have on the autonomics
dec GI motility | postural hypotension

Pathophys (15 decks)

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