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old patho 154 > Endocrine disorders and diabetes > Flashcards

Endocrine disorders and diabetes Flashcards

1
Q

what are the basic problems of endocrine disorders

A
  • hypersecretion (inc hormone (H) production)
  • hyposecretion (dec or no H production)

these result in inappropriate target cell responses

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2
Q

where are hormones sites of actions. how are they specific?

A

their sites of action arent where theyre released

they have specific target cells with surface receptors for the H. when the H binds it acts

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3
Q

etiology of hypofunction

A

-in order to synthesize hormones you need reactants and enzymes. eg to make thyroid hormones you need iodine

  • dietary deficiency
  • metabolic defect (eg missing enzyme)
  • receptor defect
  • immune disorder (eg T cells causing damage)
  • no trophic stimulation->atrophy (we need trophic stimulation for H release)
  • Tx for hypersecretion
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4
Q

etiology of hyperfunction

A
  • inc trophic stimulation (negative feedback control is nec for H balance)
  • defect in negative feedback
  • secretory tumors (this could occur with a tumor which may initially resemble the tissue of origin. In the early stages of dev it might secrete something eg a H. This tumor may not always be in the gland, it can be ectopic-located elsewhere)
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5
Q

what is the most common endocrine disease

A

dm

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6
Q

RISKS FOR diabetes ARE SIMILAR TO the risks for

A

CVD

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7
Q

is the pancreas more endocrine or exocrine

A

its 99% exocrine

1%, the islets of langerhans produce hormones

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8
Q

GLUCAGON

is produced by

A

produced by alpha cells in the islets of langerhans of the pancreas released when blood glucose is low

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9
Q

insulin
is produced by
action

A

produced by the beta cells in the islets of langerhans of the pancreas released when blood glucose is high

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10
Q

third hormone produced by the pancreas

is it only produced in the pancreas

A

somatostatin

it is produced elsewhere in GI system and nervous system

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11
Q

DM is a disorder of…

A

insulin action or secretion which causes widespread metb problems with proteins, carbohydrates and lipids

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12
Q

action of glucagon

A

It stimulates the conversion of stored glycogen (stored in the liver) to glucose which can be released into the bloodstream. This process is called glycogenolysis.

It promotes the production of glucose from amino acid molecules. This process is called gluconeogenesis.

It reduces glucose consumption by the liver so that as much glucose as possible can be secreted into the bloodstream to maintain blood glucose levels.

Glucagon also acts on adipose tissue to stimulate the breakdown of fat stores into the bloodstream.

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13
Q

action of insulin

A

action: gives ability to metabolize carbohydrates, fats, and proteins to store glucose in the liver and to convert glycogen to fat stores. Inhibits the production of glucose by the liver

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14
Q 
function of somatostatin. 
how is it controlled?
A

inhibits the secretion of growth hormone, TSH, glucagon, and insulin.
it also dec GI motility and secretion

negative feedback with the hormones it inhibits

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15
Q

what is diabetes mellitus

A

a disorder of insulin action or secretion which causes widespread metb problems with CHO, proteins, lipids

it is an absolute or relative insulin deficiency that leads to compromized glucose homeostasis

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16
Q

what occurs with absolute deficiency of insulin vs reltive

A

the beta cells are damaged in absolute.

in relative deficiency the beta cells are intact but there is a problem at the target cell level

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17
Q

which body systems are most affected by complications that can arise form DM

how serious are these complications

A

CV, ocular, renal, neuro

both the acute and chronic complic are life-threatening if uncontrolled

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18
Q

how is DM classified
which is most common

how is type 1 further broken down

A

into Type 1 (10%) and Type 2 (90%)
others such as gestational, drug induced…

Type 1A is immune based (90-95% of cases). the remaining 5-10% are 1B and idiopathic

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19
Q

etiology of DM in general

A

complex trait (polygenic and environmental factors

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20
Q

etiology of Type 1 DM

A
  • familial (10x inc risk)
  • “insulin gene” on Chr 11 (10% of those w type 1 have this) the insulin gene codes for proteins that regulate the fx of Beta cells
  • MHC genes on Chr 6 (40%) causes self targeting
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21
Q

what is Type 2 in young people called.

what is wrong with this term?

A

MODY-mature onset diabetes in the young

it is contradictory

in the past when there wasnt access to so much junk food Type 2 Dm occurred in the 40s+ but is now occurring early d/t poor lifestyle, inacitivy etc

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22
Q

etiology Type 2 DM

A

etiology isnt clear cut
50% is d/t glucokinase gene on Chr 7

once glucose enters the cell its phosphorylated to keep it inside the cell for metabolism. Glucokinase is the enzyme that phosphorylates it.

for people with Type 2 Dm the glucose wont stay in their cell and they cant metb it so they get hyperglycemia

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23
Q

what is prediabetes

what are good measures to show whether someone is prediabetic. Where would the results be

A

it is a metabolic stage that progresses to diabetes.

impaired fasting glucose (6.16.9mmol/L)
impaired glucose tolerance (7.8-11mmol/L)
HbA1C (6-6.4%)

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24
Q

what is IFG and how would it appear if prediabetic

A

it is when you have an IFG (impaired fasting glucose) of 6.1-6.9mmol/L which is higher than normal. Normal max should be 5.5.

for this procedure you get the pt to fast (usually overnight). You are putting them into the post-absorptive state.

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25
Q

how would you get an IGT

A

fast the pt overnight. Before they take in any food/glucose you measure their blood glucose. Their blood glucose will inc after they take in glucose (15min after) The beta cells will release insulin to dec BG. IF this doesnt happen and BG is still high it indicates impaired GT.

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26
Q

what is HBA1C. what is a normal value vs a prediabetic value

A

1C is a subclass of adult HB which has the highest affinity for glucose. When you have elevated blood glucose the glucose will irreversibly bind to all proteins in the blood such as HbA. When the glucose binds to any protein it makes it dysfunctional.

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27
Q

what is metabolic syndrome

A 
it predisposes pts to Type 2 DM and CVD
some features
-IFG
-IGT
-I resistance
-HTN
-abdominal obesity 
-hyperlipidemia
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28
Q

abdominal obesity and metabolic syndrome
measures for males that indicate metabolic syndrome
for women

if it is this number what is this called

A

women >88cm+=diabesity

for men >102cm is diabesity

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29
Q

would someone with type 2 diabetes have metabolic syndrome

A

most likely yes

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30
Q

type 1 DM usually occurs ____
d/t
is

A

-usually early age onset
-autoimmune
genetic predisposition
env triger (virus??) not sure which virus
-progressive destruction of beta cells
up to 90% destroyed
absolute insulin def
-Insulin and islet cell autoAB produced

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31
Q

in Type 1 Dm why do autoAB form?

A

d/t the preceding viral infection

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32
Q

what is insulitis and why would this occur.

if a pt had this what kind of cells might be visible histologically

A

inflm of the beta cells in the islets of langerhans.

this could occur fromt he autoab that arise i Type 1 DM and whenever you have autoimmunity there are T cells present.

Histologically you would see Tc cells int he Islets of Langerhans

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33
Q

Type 2 DM
beta cells?
what is happening with insulin levels? release? response? etc?
worse than type 1?

A

-beta cells are mostly intact
-there is a relative insuin def
delayed secretion
defective target cell response
insulin resistance “absence of a hypoglycemic -response during states of hyperglycemia”
-insulin levels can be normal, high or low
-less severe form than Type 1

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34
Q

where there is tissue destr what protein will deposit?

A

amyloid

35
Q

in the face of hypoglycemia how does the liver respond

A

it rel glucose through glycogenolysis

36
Q

what is a renal threshold

what is it for glucose. what would happen if it were 5mmol/L greater than this

A

the conc of a compound or solute in blood above which that compound will appear int he urine

10mmol/L

if it were 15mmol/L conc in blood then 5mmol/L would appear in the urine

37
Q

what are the 3 processes involved in urine formation

A

filtration
active secretion
reabsorption

38
Q

how does a hyperglycemic get dehydrated

what might dehydration lead to

A

glycosuria->inc osmotic pressure in the filtrate->fluid enters filtrate->polyuria->glucose inc conc of solute->draws fluid into urine->dehydration which may lead to polydipsia (excessive thirst and intake)

ketonuria may contribute to the dehydration by pulling more fluid if it is bad enough

39
Q

patho of diabetes (T1, T2)

A
  • I def->impaired glucose utilization and inc hepatic glucogenesis->hyperglycemia (11-67mmol/L->renal threshold is exceeded->glycosuria->osmotic pressure in filtrate inc ->fluid enters filtrate->polyuria-> dehydration->polydipsia (excess thirst and intake??)
  • d/t insulin def there is impaired glucose utilization by cells

-inc in mobilization and use of proteins and lipids ->inc protein and lipid metabolites in blood (eg ketones)
(although the body’s primary source of energy is carbs it will next mobilize lipids then protein and convert them into glucose)

-the accumulation of ketones can lead to ketoacidosis->acidotic coma and death. They can also cause ketonuria which enhances polyuria

40
Q

what part of diabetes causes hyperlipidemia

A

when you have hypoglycemia and youre mobilizing lipids and protein for energy

41
Q

mnfts of DM

A
  • polyuria
  • polydipsia
  • polyphagia (inc appetite and inc food intake)
  • weight loss (calories will be lost through urine. the weight loss is not caused by fluid loss.)
  • other complications
42
Q

acute complications of DM (3)

A
  • hypoglycemia
  • diabetic ketoacidosis
  • hyperosmolar hyperglycemic state (HHS)
43
Q

which type of Dm is more likely to experience hypoglycemia

why would this occur

A 
Type 1 
d/t:
--missed meal
--insulin OD
--exces activity
44
Q

can–missed meal
–insulin OD
–excess activity
only cause hypoglycemia in DM pts

A

no. can also cause DM in nondiabetics

45
Q

Tx fo hypoglycemia

A

mild: 15g of CHO carbs p.o.

severe (

46
Q

hypoglycemic coma

when does it occur

A

brain deprived of glucose

-LOC is deprived of

47
Q

Tx of hypoglycemic coma

A

1mg of glucagon subcu or IM

48
Q

DKA 42-11

A

diagram

49
Q

if you encounter a diabetic in coma what do

A

dont know if hyper or hypoglycemic

50
Q

what is nec for DKA to occur

A

either a severe def of I or

excess glucagon

51
Q

what are the derangements from DKA

A
  1. hyperglycemia
  2. ketosis
  3. metabolic acidosis

all of this will cause hyperglycemia. the cells cant use glucose so they use lipids which forms glycerol and is converted to glucose in liver (gluconeogenesis). the glucose enters blood but body still cant use it

it ends in circultory shock (if the fluid loss is extreme enough i assume?)

52
Q

HHS=
occurs more often in
is d/t
what happens

A

hyperosmolar hyperglycemic state
usually in T2 and elderly
d/t CHO intake and inc insulin resistance

severe hyperglycemia->hyperosmolarity->cellular fluid efflux->glycosuria->water loss->dehydration

there is no ketoacidosis

53
Q

why is there no ketoacidosis in HHS

A

lipolysis causes ketoacidosis. there is generally not a total I def as it affects usually Tpe 2 Dm

still dont really understand this

54
Q

chronic compilcations occur approx ___yrs after disease onset

A

15

55
Q

chronic complications of DM

A 
vascular damage->atherosclerosis, MI, CVA
..retinopthy
..retinopathy
..neuropathy
..infections

all the ones with dots above are underpinned by changes in the vessels

CAD
CVA
which would also be caused by vessel changes and werent n his list for some reason

56
Q

what type of infections happen w DM pt

what prevalence do infections have

A

45% prevalence

foot infections and UTIs are most common

57
Q

how do metabolites in vessels cause damage

A

when theres hyperglycemia the glucose binds to proteins in the circulation eg albumin, Hb once bound (glycosated proteins) their fx is impaired

all byproducts, glycosylate proteins and products ill bind to endothelium. When removed or bound they cause injury which leads to inflm-> thickening. This affects transcapillary exchange

58
Q

what is a glucose + a protein

A

glycosylated protein

59
Q

if there is impaired transcap exchange what happens to the blood

A

blood gets more viscous and platelets will agglutinate->impeded blood flow->impaire delivery of resources and removal of wastes. This is a local and systemic problem

60
Q

process of vascular damage d/t Dm

A

-metb is altered-> abn metabolites accum and inflict damage
-glucose + proteins-> glycosylated proteins-> nonfx
eg Hb, albumin, collagen, retinal proteins
-glycosylated proteins deposit on endothelium->impaired capillary exchange
-platelet aggregation->blood flow impeded
-impaired healing WHY d/t impaired perfusion, lack of resources and failure of adequate removal of wates
-growth of anaerobic bacteria WHY

61
Q

why is there growth of anaerobic bacteria w vascular damage in DM

A

at a tissue level eg peripheral superficial tissue level such as between the toes there is an anaerobic, hypoxic environment. There is a dec of oxygen and buildup of C02, metabolites, not enough nutrients there which allows the bact to colonize

62
Q

retinopathy as complic of DM

A

the capillary is damaged-> aneurysms->rupture->visual impairment
-cataracts and glaucoma (dev more quickly in DM)

63
Q

what are cataracts

how does Dm cause it

A

the lens is normally transparent but w cataracts the lens becomes opaque->light cant pass through as easlly. Cataracts are part of the normal aging process. It is common to replace lens.

when there is an excess of glucose it will become sorbitol which is implicated in cataracts. There is also an intermed product fructose

64
Q

what is glaucoma

A

inc intraocular pressure. It is damage to the optic nerve caused by the inc pressure. of the fluid in eyes eg vitreous humour.
It is not r/t BP

it is assoc w aging but not as common as cataracts

65
Q

nephropathy and Dm

A

glomerular damage-> dec! renal fx-> renal failure

66
Q

Neuropathy

A
  • neural ischemia
  • some demyelination (d/t ischemia and inflm)
  • poor conduction

this results in diabetics not sensing pain etc

67
Q

HTN and DM

A

40% prevalence in DM pts

  • it is both a comlication and risk factor for DM
  • it is a major risk for MI, CVA, nephropathy

the damage to the capillaries also happens in large vessels which is like atherosclerosis

68
Q

how would Dm cause MI or CAD

A

hyperlipidemia (d/t altered metb)-> atherosclerosis-> MI

69
Q

how does DM put pt at risk of CVA

A

hyperlipidemia (d/t altered metb->atherosclerosis->CVA

70
Q

why are UTIs so common in diabetics

A

d/t impeded perfusion and
-w hyperglycemia the renal threshold is exceeded which allows glucose etc into urine in bladder and is a good env for bacterial growth

71
Q

why are infections so diff to manage in Dm pt

A

-d/t vascular insuff (02, Ab, nutrients)

  • leukocytes in blood have surface proteins which the glucose may bind to and cause them to cease fx. it also diff for them to arrive to site
  • neuropathies (eg cant feel foot and are unaware of infection)
72
Q

Dx of Dm

A
  • hx (3 Ps, unexplained wt loss
  • random glucose >11mmol/L (which isnt ideal as they could have starved, just eaten etc) OR
  • IFG (greater than or equal to 7mmol/L) OR
  • IGT (>11mmol/L) OR
  • HbA1C greater than or equal to 6.5%
73
Q

how long is RBC life cycle

A

4 months

74
Q

Tx of Dm if unsure whether pt is T1 or 2 or just prediabetic what do

how do you treat prediabetic

A

differetiate 1 vs 2 by measuring insulin level

lifestyle modification for type 2 for several months which often works

75
Q

if lifestyle doesnt work as Tx for DM what next

A 
glycemic control.
   oral hypoglycemics (Type 2)
      -inc tissue response to insulin
      -stimulates beta cels
      -dec hepatic glucogenesis
76
Q

metformin is often used on its own after HbA1C of ___
after 2-3 months of lifestyle modification

what would be used for T1
what would be used if HbA1C >9%

A

7%

T1=insulin
>9% then use metformin and insulin

77
Q

why not give oral insulin

A

insulin is a protein which would get broken down into a.a in GI tract

78
Q

exocrine fx of pancreas

A

proteases
pancreatic lipase
amylase

79
Q

other than somatostatin, insulin and glucagon what H does the pancreas prod

A

Gastrin: This hormone aids digestion by stimulating certain cells in the stomach to produce acid.

vasoactive intestinal peptide

80
Q

if there are no carbs available what would the body use next as fuel

A

lipids

-inc in mobilization and use of proteins and lipids ->inc protein and lipid metabolites in blood (eg ketones)
(although the body’s primary source of energy is carbs it will next mobilize lipids then protein and convert them into glucose)

-the accumulation of ketones can lead to ketoacidosis->acidotic coma and death. They can also cause ketonuria which enhances polyuria

81
Q

what is the insulin gene and what does this affect?

A

-“insulin gene” on Chr 11 (10% of those w type 1 have an issue with this) the insulin gene codes for proteins that regulate the fx of Beta cells

82
Q

what gene causes self-targeting in Type 1 DM

A

MHC genes on Chr 6 (40%) causes self targeting

83
Q

what is glucokinase?

which type of DM is this assoc with?

how is this assoc w genetics?

what effect does this have on blood glucose?

A

50% is d/t glucokinase gene on Chr 7

once glucose enters the cell its phosphorylated to keep it inside the cell for metabolism. Glucokinase is the enzyme that phosphorylates it.

for people with Type 2 DM the glucose wont stay in their cell and they cant metb it so they get hyperglycemia

old patho 154 (18 decks)

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