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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
how would you get an IGT
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.
26
what is HBA1C. what is a normal value vs a prediabetic value
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.
27
what is metabolic syndrome
``` it predisposes pts to Type 2 DM and CVD some features -IFG -IGT -I resistance -HTN -abdominal obesity -hyperlipidemia ```
28
abdominal obesity and metabolic syndrome measures for males that indicate metabolic syndrome for women if it is this number what is this called
women >88cm+=diabesity | for men >102cm is diabesity
29
would someone with type 2 diabetes have metabolic syndrome
most likely yes
30
type 1 DM usually occurs ____ d/t is
-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
31
in Type 1 Dm why do autoAB form?
d/t the preceding viral infection
32
what is insulitis and why would this occur. if a pt had this what kind of cells might be visible histologically
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
33
Type 2 DM beta cells? what is happening with insulin levels? release? response? etc? worse than type 1?
-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
34
where there is tissue destr what protein will deposit?
amyloid
35
in the face of hypoglycemia how does the liver respond
it rel glucose through glycogenolysis
36
what is a renal threshold what is it for glucose. what would happen if it were 5mmol/L greater than this
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
what are the 3 processes involved in urine formation
filtration active secretion reabsorption
38
how does a hyperglycemic get dehydrated what might dehydration lead to
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
patho of diabetes (T1, T2)
- 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
what part of diabetes causes hyperlipidemia
when you have hypoglycemia and youre mobilizing lipids and protein for energy
41
mnfts of DM
- 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
acute complications of DM (3)
- hypoglycemia - diabetic ketoacidosis - hyperosmolar hyperglycemic state (HHS)
43
which type of Dm is more likely to experience hypoglycemia why would this occur
``` Type 1 d/t: --missed meal --insulin OD --exces activity ```
44
can--missed meal --insulin OD --excess activity only cause hypoglycemia in DM pts
no. can also cause DM in nondiabetics
45
Tx fo hypoglycemia
mild: 15g of CHO carbs p.o. | severe (
46
hypoglycemic coma | when does it occur
brain deprived of glucose | -LOC is deprived of
47
Tx of hypoglycemic coma
1mg of glucagon subcu or IM
48
DKA 42-11
diagram
49
if you encounter a diabetic in coma what do
dont know if hyper or hypoglycemic
50
what is nec for DKA to occur
either a severe def of I or | excess glucagon
51
what are the derangements from DKA
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
HHS= occurs more often in is d/t what happens
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
why is there no ketoacidosis in HHS
lipolysis causes ketoacidosis. there is generally not a total I def as it affects usually Tpe 2 Dm still dont really understand this
54
chronic compilcations occur approx ___yrs after disease onset
15
55
chronic complications of DM
``` 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
what type of infections happen w DM pt | what prevalence do infections have
45% prevalence foot infections and UTIs are most common
57
how do metabolites in vessels cause damage
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
what is a glucose + a protein
glycosylated protein
59
if there is impaired transcap exchange what happens to the blood
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
process of vascular damage d/t Dm
-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
why is there growth of anaerobic bacteria w vascular damage in DM
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
retinopathy as complic of DM
the capillary is damaged-> aneurysms->rupture->visual impairment -cataracts and glaucoma (dev more quickly in DM)
63
what are cataracts how does Dm cause it
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
what is glaucoma
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
nephropathy and Dm
glomerular damage-> dec! renal fx-> renal failure
66
Neuropathy
- neural ischemia - some demyelination (d/t ischemia and inflm) - poor conduction this results in diabetics not sensing pain etc
67
HTN and DM
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
how would Dm cause MI or CAD
hyperlipidemia (d/t altered metb)-> atherosclerosis-> MI
69
how does DM put pt at risk of CVA
hyperlipidemia (d/t altered metb->atherosclerosis->CVA
70
why are UTIs so common in diabetics
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
why are infections so diff to manage in Dm pt
-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
Dx of Dm
- 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
how long is RBC life cycle
4 months
74
Tx of Dm if unsure whether pt is T1 or 2 or just prediabetic what do how do you treat prediabetic
differetiate 1 vs 2 by measuring insulin level lifestyle modification for type 2 for several months which often works
75
if lifestyle doesnt work as Tx for DM what next
``` glycemic control. oral hypoglycemics (Type 2) -inc tissue response to insulin -stimulates beta cels -dec hepatic glucogenesis ```
76
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%
7% T1=insulin >9% then use metformin and insulin
77
why not give oral insulin
insulin is a protein which would get broken down into a.a in GI tract
78
exocrine fx of pancreas
proteases pancreatic lipase amylase
79
other than somatostatin, insulin and glucagon what H does the pancreas prod
Gastrin: This hormone aids digestion by stimulating certain cells in the stomach to produce acid. vasoactive intestinal peptide
80
if there are no carbs available what would the body use next as fuel
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
what is the insulin gene and what does this affect?
-"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
what gene causes self-targeting in Type 1 DM
MHC genes on Chr 6 (40%) causes self targeting
83
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?
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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