Endocrine disorders Flashcards
2 Basic problems for endocrine disorders
hyperfunction
hypofunction
Hyperfunction
increase in hormone secretion/action
Hypofunction
decrease or no hormone secretion or action
Hypofunction etiology
- dietary deficiency
- metabolic defect
- no trophic stimulation cause atrophy
- receptor defects (distorted or damaged shape)
- suppresive therapy (surgery/Tx for hypersecretion)
- immune disorders (anitbodies bind to receptor sites)
Hyperfunction etiology
- excessive trophic stimulation
- defect in negative feedback loop leads to no suppression
- Secretory tumor ( tumor cells will be same so have same secretion)
ectopic tumor
located somewhere else ex. cell in lung that secretes hormone
non functioning tumor
destroys normal secretory cells that can lead to hypofunction
commonest endocrine disorder, affects approx
diabetes mellitus (2.5 mil)
diabetes mellitus has ______ or ________ insulin defects
absolute or relative
absolute insulin defects
no insulin produced
relative insulin defects
insulin produced not able to recognize
Diabetes mellitus is a complex disease that affects
protein metabolism, lipid metabolism and carbohydrate metabolism
Diabetes melliuts has defective
insulin secretion or action which leads to widespread metabolic defects (proteins, carbohydrates & lipids)
Diabetes melliuts is ________ if uncontrolled
life threatening
Impact of diabetes
Cardivascular, occular, renal, nueroimplications
these will develop approx 10 yrs, with better management takes longer to dev, with bad management happens sooner
classification of diabetes has 2 types
- type 1
- type 2
Type 1 affects
10 % of individuals with diabetes
Type 2 affects
90% of individuals with diabetes
Type 1 is __________ insulin deficiency
absolute, destruction of cells that create insulin (beta cells)
Type 1a
Type 1b
1a (immune mediated 90-95%)
1b (idiopathic destruction of beta cells 5-10%)
Type 2 beta cells are
intact and it is relative insulin deficiency
Etiology of both type 1 and type 2
complex trait (polygenic + environmental) enivormental ex. viral infection & obesity
Type 1 has
juvenile onset (early onset)
LADA
progressive form of type 1
latent autoimmune diabetes in adults
MHC genes
-majorhistocompatability complex code for cells to be able to identify as self to immune system
Type 1 etiology (genes) & others
- MHC genes on chromosome 6 (40%)
- Insulin gene on chromosome 11 (10%) -function division of beta cells
- T cell hypersensitivity to Beta cell antigen
- familial risk (increase x10)
Type 2 is Mo
mature happens later in life
MODY
maturing onset diabetes in young -this is a growing condition
Type 2 etiology
-50 % due to glucokinase gene on chr 7
Glucokinase
adds phosphate to glucose catalyze by enzyme glucokinase. therefore glucose cannot stay in cell and moves out
Prediabetes
metabolic stage before onset of DM
prediabetes has an imparied
- impaired fasting glucose
- Abnormal oral glucose tolerance test
- increase
several characteristics of Metabolic syndrome
- abdominal obesity w > 88 m >102
- HTN
- hyperlipidemia (increase LDL, Low HDL, High triglycerides)
- impaired fasting glucose
- Impaired glucose tolerance
- Insulin resistance (insulin present but can’t do job)
insulin resistance
absence of hypoglycemic response to hyperglycemia in the presence of insulin
Type 1 diabetes is a progressive autoimmune destruction of
beta cells up to 90 % of cells are destroyed
type 2 diabetes beta cells
intact, but dysfunctional no autoimmunity
Type 2 diabetes, relative insulin deficiency from:
- Insulin resistance
- Deranged secretion (may have less secretion than needed)
- Defective target cell response
- hepatic glucogenis
Type 2 diabetes has has ____, _____ or _____ in insulin levels
normal, increase or decrease
need insulin to move _____ into cells
glucose
Patho of Type 1 & Type 2 Diabetes
- insulin deficiency
- impaired glucose utilization & increase in hepatic gluconeogenesis
- Hyperglycemia (11-67mmol/L)
- renal threshold exceeded
- glucosuria
- increase in osmotic pressure in filtrate
- fluid enters filtrate
- polyuria
- dehydration
- polydipsia (
Manifestations of diabetes
- polyuria & (frequencey)
- Polydipsia
- Polyphagia
- wt loss (type 1)
- obesity (type 2)
- complications
polyuria
excessive peeing
polydipsia
excessive thirst
polyphagia
excessive hunger, hungry all the time (losing all calories in urine)
glucosuria
Increased glucose in urine
The 3 acute complications of diabetes (life threatening):
- Diabetic ketoacidosis (DKA)
- Hyperosmolar hyperglycemic state (HHS)
- Hypoglycemia leading to Hypoglycemic coma
Diabetic ketoacidosis usually happens in type _____
1
Diabetic ketoacidosis
- severe insulin deficiency (can’t take glucose into cells)
- glucagon excess (hormone that breaks glycogen in glucose)
3 main features of diabetic ketacidosis
- hyperglycemia
- ketosis (formation of ketones)
- metabolic acidosis
glucogenesis
formation of carbohydrate from non-carbohydrate sourve
Hyperosmolar hyperglycemic state is more common in
Type 2 and elderly
Hyperosmolar hyperglycemic state is due to
- increase in insulin resistance
- excessive increase in carbohydrate intake (or if don’t take oral meds)
Hypoglycemia usually in type
1
Hypoglycemia due to
- insulin overdose (double dose of insulin or oral meds)
- missed meal
- overexertion
Hypoglycemia is a blood glucose level of
less than 4 mmol/L
Hypoglycemia causes
altered cerebral function and activation of ANS
Treatment of Hypoglycemia
- 15g - 20g Carbohydrates po
- inject glucagon
Hypoglycemic coma
- brain depends exclusively on glucose for metabolic needs
- brain cells are insulin independent
- brain deprived of glucose
- loss of consciousness
Brain cells are_____independent
Brain cells are insulin independent (can take in glucose without insulin)
erythrocytes are also insulin independent
Treatment of Hypoglycemic coma
- 1mg glucagon subcut or IM
- 20-50 ml 50 % glucose IV
chronic complications of diabetes are due to
metabolic changes & vascular damage
Chronic complications of diabetes
- microvascular
- macrovascular
- CAD & MI
- CVA (stroke)
- PVD
- infections (particularly foot & UTI)
Microvascular complications of diabetes
- retinopathy
- nephropathy
- neuropathy
glycosylated protiens
glucose + protien
