1/22
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
Give examples of:
Polysaccharide
Disaccharide
Monosaccharide
Reducing sugars
Nonreducing sugars
Polysaccharide: starch, glycogen, cellulose (>10 monosaccharides)
Disaccharide: sucrose, lactose, maltose
→glu +glu = maltose
→glu + fruc = sucrose
→glu + galactose = lactose
Monosaccharide - glucose, galactose, fructose
Reducing sugars - glucose, maltose, lactose, galactose, fructose
Nonreducing sugars - sucrose
*pancreas and salivary gland = amylase
*gut = sucrase, lactase, maltase
only hypoglycemic hormone, beta cells of islets of langerhans of pancreas
Insulin

Insulin
released when glucose are high
stored in liver, fat muscle
reciprocal relationship with glucagon
_ = false decrease because of degrading enzyme in RBC
_ - carbohydrates to fatty acids
normalization of glucose: _
released when glucose are high
stored in liver, fat muscle
reciprocal relationship with glucagon
HEMOLYSIS = false decrease because of degrading enzyme in RBC
LIPOGENESIS - carbohydrates to fatty acids
normalization of glucose: <2 HOURS

HYPOGLYCEMIA
decrease glucose levels - _
criteria for diagnosis of hypoglycemia: _
drug administration cause: (3)
critical illness: (3)
hyperinsulinism: _
autoimmune hypoglycemia - insulin autoantibodies
non beta cell tumors: (3)
hypoglycemia of infancy and childhood: (3)
Alimentary (reactive) hypoglycemia: (2)
Idiopathic (functional) postprandial hypoglycemia
DIAGNOSTIC TEST: _
decrease glucose levels : < 0r equal to 60 mg/dL
criteria for diagnosis of hypoglycemia: WHIPPLE'S TRIAD (hypoglycemia > intake of glucose > alleviation of symptoms)
drug administration cause: INSULIN, SALICYLATES, ALCOHOL
critical illness: SEPSIS, HEPATIC, RENAL FAILURE
hyperinsulinism: CANCER
autoimmune hypoglycemia - insulin autoantibodies
non beta cell tumors: LEUKEMIA, LYMPHOMA, HEPATOMA
hypoglycemia of infancy and childhood: GALACTOSEMIA, REYE'S SYNDROME, GSD
Alimentary (reactive) hypoglycemia: POST-GASTRIC SURGERY, within 4 hours after eating meal
Idiopathic (functional) postprandial hypoglycemia
DIAGNOSTIC TEST: 5-HOUR GTT (hypoglycemic dip is not seen until after 3 hours, there should not be dip in glucose levels before 3 hours)
primary hyperglycemic agent synthesized by alpha cells of pancreas
glucagon
Hyperglycemic agents
GAGCHETS
G - glucagon
A - acth
G - growth hormone
C - cortisol
H - human placental lactogen
E - epinephrine/norepinephrine
T - thyroxine / T4
S - somatostatin
Actions of glucagon
gluconeogenesis
glycogenolysis
lipolysis
Actions of Insulin
Glycolysis
Glycogenesis
Lipogenesis
HYPERGLYCEMIA
hallmark sign of DM I and II
FBS level: _
Causes: _
FBS level: >126 mg/dL
Causes:
→ stress, severe infection, dehydration, pregnancy, hemochromatosis, pancreatectomy, abnormal insulin receptor, insulin deficiency
Iron accumulation in pancreas =
bronze diabetes mellitus
Diabetes Mellitus
diabetes in greek: _
mellitus in latin: _
diabetes in greek: to siphon or pass through
mellitus in latin: sweet
Type 1 DM
Former names
Insulin-dependent DM
Juvenile Onset Diabetes Mellitus
Brittle Diabetes
Ketosis-prone diabetes
Type 1 DM
Pathogenesis: _
Peak incidence: _
Beta cell destruction, insulinoipenia
Most common: autoimmune disorder
Peak incidence: childhood and adolescence
Type 1 DM
C-peptide
→reliable indicator for pancreatic surgery and insulin secretion
low
Type 1 DM
symptoms
develop abruptly - polyuria, polydipsia, polyphagia
rapid weight loss
complications: microvascular disorders - nephropathy, neuropathy, retinopathy
Type 1 DM
Ketones/Ketosis
High/Uncontrolled
Ketone Bodies
can be used by the brain for energy thru _
Forms: (3)
can be used by the brain for energy thru TRICARBOXYLIC ACID CYCLE (KREB'S)
Forms: (3)
→Beta-hydroxybutyrate (78%) - major
→Acetoacetic acid (20%)
→Acetone (2%)
Type 1 DM
associated with HLA-_
autoantibodies present: (4)
associated with HLA-DR3 and HLA-DR4
autoantibodies present:
→islet cell autoantibodies
→insulin autoantibodies - common in children
→glutamic acid decarboxylase (GAD65) autoantibodies
→tyrosine phosphatase IA-2 and IA-2B autoantibodies
Type 1 DM
Medication
Insulin
Type 2 DM
Former names
Non-insulin dependent diabetes mellitus
Adult type/maturity onset diabetes melitus (>40)
Stable diabetes
Ketosis-Resistant Diabetes
Receptor-deficient DM
GENETICIST'S NIGHTMARE
Type 2 DM
Pathogenesis
insulin resistant
associated with obesity and sedentary lifestyle, PMOS, hypertensiion
Type 2 DM
C-peptide
low
Type 2 DM
symptoms
milder symptoms than type