midterm physio deck 4

Question 1

insulin dependent tissue

Answer 1

muscles and adipose

Question 2

protein sparing effect of ketones

Answer 2

as ketone production rises, they are used increasingly by the CNS as a fuel –> spares breakdown of muscle in survival situations

Question 3

glycogen vs fat as storage efficiency

Answer 3

glycogen is inefficient since each gram requires 1-2 g of intracellular watervsfat that is a water free environment

Question 4

islet cells and their roles

Answer 4

alpha - glucagon secretingbeta - insulin secretingdelta - somatostatin (SRIF) secreting

Question 5

what cells secrete glucagon?

Answer 5

alpha cells of islet pancreas

Question 6

SRIF (somatostatin) actions

Answer 6

all actions of somatostatin are INHIBITORYinhibits TSH and GH in pituitaryinhibits insulin and glucagon release in pancreatic islet cells

Question 7

insulin circulates _____what enzyme breaks it down?

Answer 7

free in plasmaglutathione transhydrogenase (breaks all three disulfide bonds)

Question 8

does insulin cross placenta?

Answer 8

no

Question 9

insulin receptor is what type?

Answer 9

tyrosine kinase that autophosphorylates

Question 10

do insulin receptors use cAMP?

Answer 10

no, it is not a messenger for insulin stimulationtyrosine kinase does notcAMP actually goes down

Question 11

malonyl coA and insulin

Answer 11

insulin enhances malonyl coa production in hepatocytesmalonyl coa then inhibits the transport of free FA into mitochondria so ketoacids arent made; allows FA biosynthesishigh malonyl coa = low ketogensis

Question 12

glucagon receptor

Answer 12

Gs protein linked to adenylate cyclase

Question 13

is there a backup for insulin?

Answer 13

NO

Question 14

is there a backup for glucagon?

Answer 14

yes4 other catabolic hormones = norepi, epi, cortisol, and GHall correct for hypoglycemiaglucagon and catecholamines are short termcortisol and GH are longer term adaptation

Question 15

obesity results in what kinds of state?basis for what?

Answer 15

chronic, low grade systemic inflammationbasis for t2 diabetes insulin resistance–elevated levels of pro-inflammatory cytokines act to down regulate insulin receptors

Question 16

what triggers pro-inflammatory cytokines in obesity?

Answer 16

adipocytes accumulatelipid stores increase in sizeincreased distance oxygen must diffuse cells become hypoxic and upregulate cytokine expressionattracts monocytes and activated into macrophagesleads to systemic proinflammatory state with generalized insulin resistance

Question 17

type1 vs type 2which is dependent on insulintreatment?

Answer 17

type 1 is insulin dependent - give insulintype 2 is insulin independent - give oral hypoglycemics

Question 18

2 main mechanisms for Diabetes pathogenesis

Answer 18

1) glycation - exposure of proteins to high glucoseresults in unregulated nonenzymatic glycation –> disrupts structure and function and can cause modified proteins to elicit autoimmune attack on native protein***glycated Hb is a good assessment of glycemic control since Hb has life of 120 days2) accumulation of sorbitol - sorbitol is formed by reduction of glucose by aldose reductase which is activated in diabetics

Question 19

diabetic microangiopathy

Answer 19

BM thickening in small vesselsmech: hyaline like glycoprotein accumulates in BM resulting in dilation and increased permeabilitycauses retinopathy, neuropathy, and nephropathy w proteinuria and renal failure

Question 20

diabetic macroangiopathy

Answer 20

progressive occlusion of arteriesleads to angina, MI, claudication, gangrene, ischemic attacks and cerebral infarction

Question 21

diabetic neuropathy

Answer 21

symmetric sensory loss in distal extremities

less sensation, tingling/burningautonomic = orthostatic hypotensions and GI/urogenital motor distrubances

Question 22

DKA

Answer 22

diabetic ketoacidosisinsulin deficiency resulting in metabolism disturbances with hyperglycemia and metabolic acidosis due to accumulation of ketoacids, acetoacetic acid, and beta hyroxybutyrateusually glucagon is greatly increased exaccerbating the absence of insulin

Question 23

DKA mechanism

Answer 23

insulin lack decrease in glucose useliver and muscle glycogenolysis; increased ketogenesishyperglycemialimited ketone body utilization by peripheral tissueglycosuria and osmotic diuresis –> water and electrolyte loss/vomitingdehydration and hemoconcentrationhypotension and decreased renal blood flow; CV depressionanuria/shockcoma/death

Question 24

DKA effects on lipis

Answer 24

allows unimpeded lipolysis –> elevated plasma free FAs =more ketogenic substratein absence of insulin, hormone sensitive lipase isnt inhibited and continues to break down adipose

Question 25

DKA and CPT1/maolnyl coa

Answer 25

CPT1 is usually inhibited by malonyl coalow insulin/high glucagon –> decrease in malonyl coa –> CPT1 is no longer inhibited and ketogenesis runs uninhibited!!!

Question 26

DKA treatment

Answer 26

isotonic saline immediately for fluids!start insulin therapy next slowly and carefully until acidosis is correctedwith electrolytes/ potassium to move potassium back into cellsexogenous glucose/dextrose given to cover the insulin needed to reverse the ketosis

Question 27

DKA diagnostic criteria

Answer 27

diabetes symptoms and random plasma glucose > 200orfasting plasma glucose > 126or2 hr plasma glucose >200 during glucose tolerance testor Hba1c >6.5DKA = hyperglycemia (>200), Ketonemia/ketonuria, acidosis (ph

Question 28

clinical features of DKA

Answer 28

polyuria, polydipsia, polyphagia, and nocturiaweightlossketoacidosis: abd pain, N/v, mental changefatigue and weaknessblurry visiongenital yeast infections

Question 29

why do you need to be careful treating DKA w fluids?

Answer 29

large fluid shifts are a concern for cerebral edema

Question 30

if serum K is abnormal, do a _____

Answer 30

EKG

Question 31

cerebral edema

Answer 31

can occur 4-12 hrs after treatment startedcriteria = alterned MS/consiousness, sustained HR deceleration, and age inapropriate incontinence

Question 32

warning signs of cerebral edema

Answer 32

headache, slowed HR, neuro change (irritable, drowsy), CN palsies, rising BP, decrease O2 stats

Question 33

diagnostic features of cerebral edema

Answer 33

adnormal motor/verbal response to paindecroticate or decerebrate posturecranial nerve palsy (3,4, 6) abnormal neurogenic respiratory pattern

Question 34

treatment for cerebral edema

Answer 34

3% saline or mannitolelevate head of bedreduce fluid rate by 1/3intubation and head CT after treatment initiated

Question 35

do not ____ insulin during DKA/cerebral edema treatment

Answer 35

lowerif glucose falls, just add glucose

Question 36

pros/cons of NPH and regular insulin

Answer 36

pros: 2-3 shots per day, cheaper; less carb countingcons: strict dietary plan, less flexible or physiologic

Question 37

pros/cons of basal/ bolus (detemir/glargine and aspart)

Answer 37

pros: more physiologic, flexible, and less hypoglycemiacons: labor intensive, carb counting and atleast 4 injections per day

Question 38

how basal/bolus works

Answer 38

basal = detemir or glargine at 50% of TDDbolus = aspart(novolog) based on insulin to carb ratioTDD = .5 units/kgratio = 450/TDDcorrection factor = 1800/TDDbolus dose needed= (carbs/carbs ratio) + (BG-target)/CF

Question 39

how does exercise help diabetic

Answer 39

increases sensitivity to insulin and helps control blood sugarhave snacks available; dont exercise if ketones are present

Question 40

when diabetic person is ill…

Answer 40

DONT stop insulin - insulin req is often greater with illnesswill need extra insulin to clear ketonesdrink fluids with sugar if hypoglycemic