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SOM 204: GROWTH, REPRODUCTION AND ENDOCRINE GLANDS > WEEK 1:CLINICAL DIABETES > Flashcards

WEEK 1:CLINICAL DIABETES Flashcards

(93 cards)

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1
Q

What is diabetes Mellitus?

A

Its a chronic condition characterized by hyperglycemia due to inability of the body to produce, insulin resistance or both

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2
Q

Name the hormones that are used to regulate glucose levels in the body

A

*DECREASE: Insulin
*INCREASE: Glucagon. cortisol, epinephrine and growth hormone

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3
Q

State the types of diabetes

A

*Type 1 and 2 diabetes mellitus, Ketone prone diabetes, gestational diabetes, secondary diabetes mellitus, LADA( Latent Autoimmune Diabetes of Adults), MODY( Maturity Onset Diabetes of Youth)

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4
Q

What are the other names used for Type 1 Diabetes Mellitus?

A

*Insulin Dependent Diabetes Mellitus (IDDM)
*Juvenile Onset Diabetes mellitus

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5
Q

What are the other names used for Type 2 Diabetes Mellitus?

A

*adult Onset Diabetes mellitus
*Non-insulin Dependent Diabetes Mellitus(NIDDM)

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6
Q

State the secondary causes of diabetes mellitus

A

Chronic pancreatitis, Anti-hypertensive drugs, acromegaly, cancer, cushing’s syndrome, thyrotoxicosis

*Cushing’s syndrome is a rare endocrine disorder caused by chronic exposure of the body’s tissues to excess levels of cortisol—a hormone naturally produced by the adrenal gland.

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7
Q

Define etiology

A

the cause, set of causes, or manner of causation of a disease or condition

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8
Q

State the etiology of Type 1 Diabetes Mellitus

A

*Autoimmune disease: selective destruction of beta cells by the T lymphocytes
*Environmental factors: Viruses: rubella, coxsackie and mumps Or nutrients: cow milk

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9
Q

State the etiology of Type 2 Diabetes Mellitus

A

Insulin resistance and beta cell dysfunction

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10
Q

Differentiate Type 1 and 2 Diabetes Mellitus
AGE OF ONSET:
PATHOGENESIS
FAMILY HISTORY
DKA
OBESITY
CLINICAL PRESENTATION
TREATMENT

A

TYPE 1:Less than 30yrs, insulin deficiency, not strong, present, patient usually thin, 3p’s , DKA, weight loss

TREATMENT; Insulin, diet and exercise

TYPE 2: More than 40yrs, insulin resistance or sometimes coupled with insulin deficiency, strong, not common, common, polyuria and fatigue ( usually asymptomatic)

TREATMENT: diet, exercise, oral anti-diabetics, insulin

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11
Q

State the symptoms of diabetes mellitus

A

3P’S , weight loss, fatigue, ketones in urine, glucosuria, blurred vvision, slow wound healing, dehydration, DKA, dry skin,

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12
Q

State the causes and risk factors of developing diabetes mellitus

A

family history, obesity, poor diet, prolonged and habitual physical inactivity, polycystic ovary syndrome, cancer, Non-alcohol liver disease, alcohol abuse, acromegaly, medication, infections, cushing’s syndrome

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13
Q

State the acute complications related to diabetes mellitus

A

*hypoglycemia, DKA and HHNS

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14
Q

What does HHNS stand for?

A

Hyperosmolar Hyperglycemic Non-ketonic Syndrome

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15
Q

What are the main causes of chronic complications of diabetes?

A

Atherosclerosis damage to small blood vessels, damage to large blood vessels and inflammation

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16
Q

State the microvascular chronic complications related to diabetes

A

nephropathy, neuropathy, retinopathy

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17
Q

State the macrovascular chronic complications related to diabetes

A

diabetic foot, stroke, coronary heart disease
NON VASCULAR
Erectile dysfunction,skin problems, muscles and bones problem

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18
Q

Describe how feeding children cow milk can be a cause/ risk factor of diabetes mellitus

A

Antibodies against cow insulin closely resemble human insulin therefore it may affect beta cells

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19
Q

State the signs and symptoms of DKA

A

*Nausea: Stimulation of the CTZ by ketone bodies
*Kussmaul breathing: deep and rapid breathing ton try and clear carbondioxide and reduce chances of carbonic acid formation
*dehydration
*Polyuria
*polydypsia
*Polyphagia
*glucosuria
*Ketone in urine (ketouria)
*Abdominal pain: irritation by the acidity ( low pH)
*Weight loss
*fruity breath: due to the volatile sweet smelling acetone from acetoacetate breakdown
*Arrythmia
*dry mouth

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20
Q

State the causes of DKA

A
  • Prolonged fasting/starvation
    *Low insulin
    *low blood glucose level
    *over exercising
    *Diet restricting carbohydrates (Atkin’s meal)
    *Uncontrolled diabetes mellitus
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21
Q

Where are ketone bodies made?

A

In the liver

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22
Q

What parts of the body mainly uses ketones in post absorptive state?

A

Brain, skeletal muscles

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23
Q

Outline how ketones bodies are formed

A

*Beta oxidation of fatty acids to form acetyl CoA
* 2 Acetyl CoA’s join together by the Acetyl CoA transferase (thiolase) forming acetoacetyl CoA
*HMG CoA synthase acts on acetoacetyl CoA to form HMG CoA
*HMG CoA acted on by HMG CoA lyase to form acetacetate
*Acetoacetate acted on by beta hydroxybutyrate dehydrogenase to form beta hydroxybutyrate
Acetoacetate can also be acted on by Acetoacetate decarboxylase forming Acetone

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24
Q

Name the 3 ketone bodies produced during ketosis

A

*Acetone
*Acetoacetate
*Beta hydroxybutyrate

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25
Name the ketone body that is not acidic
acetone
26
Which ketone body is produced in large amount?
*Beta hydroxybutyrate
27
State the signs and symptoms of HHNS
Polyuria, polydypsia , dehydration, fatigue
28
Differentiate between DKA and HHNS
DKA: Low pH HHNS: Normal pH DKA: Ketone HHNS: No ketones DKA: Hyperglycemia ( greater than 300mg/dL) HHNS: Heavy duty hyperglycemia ( greater than 600mg/dL)
29
What is the conversion factor between mM and mg/dL?
1mM=18mg/dL
30
What is diabetes insipidius?
A disorder characterized by deficiency of ADH or its action resulting in polyuria
31
Describe ADH under the following headings *Where is it produced? *Where is it stored? *Function?
*hypothalamus *Posterior pituitary gland *regulate the water balance in the body by controlling amount of water kidneys reabsorb while filtering waste out of the blood
32
State the 3 types of diabetes insipidius
*Central diabetes insipidius: problemin the hypothalamus or damaged tothe pituitary gland *nephrogenic diabetes insipidius: kidney problem *Gestational diabetes insipidius : enzyme in pregnancy that destroy ADH
33
State the causes of diabetes insipidius according to their types
*Central DI: brain tumor, head injury, cell mediated immunity *Nephrogenic DI: chronic kidney disease, blocked urinary tract, medications such as lithium and tetracycline
34
State the risk factors for diabetes insipidius
*Pregnancy with more than one child *Family history *low potassium and high calcium ions in the body
35
State the possible treatment for Diabetes Insipidius
Thiazide diuretic NSAID Desmopressin
36
Name the drug given to patients with Central DI that acts like ADH
Desmopressin
37
State the signs and symptoms of diabetes insipidius
Polyuria, polydipsia,thirst, Anorexia, constipation Hyperthermia and lack of sweating Hypernatremic dehydration Nocturia: waking up at night to urinate
38
How is polyuria in diabetes insipidius different from that in diabetes mellitus?
In DI the urine is dilute
39
Describe the test for diabetes insipidius
* Check osmolality of the urine * Water deprivation test
40
State the signs and symptoms of hypoglycemia
Slurred speech, blurred vision, shaking, sweating, tachycardia, hyperventilation, convulsions, mental confusion, fatigue
41
What is HbA1C? What is the normal results for a healthy person ?
It is the amount of glucose bound to hemoglobin for the past 2 to 3 months Diabetes: 6.5% + Pre-diabetes: 6-6.5% Normal: less than 6%
42
Describe the Oral glucose tolerance test for diabetes mellitus
Drink a sugary drink made up of 75g of glucose and 300ml of water after an overnight fast. Glucose test is done in the blood after several hour. A blood glucose more than 11mM or 200mg/ dL indicate diabetes Pre diabetes:5.6-6.9/ 100-125mg/ dL
43
State the glucose levels for a fasting and post prandial glucose for a normal and diabetes mellitus patient
FASTING Normal: 3.9-5.5 Diabetes: more than 7 POST PRANDIAL Normal: less than 7.8 Diabetes: more than 11.1
44
Which part of the body is able to take in glucose without the need for Insulin during exercise?
Skeletal muscles
45
State the stimulus for insulin production?
* high blood glucose * High blood amino acids * High blood fatty acids * GI hormones ( secretin,gastrin incretins( GLP1 and GIP) Glucose like peptide 1 and Glucose like insulinotropic peptide
46
What does NEEDS stand for in the management of diabetes mellitus?
Nutrition Exercise Education Drugs Self monitoring
47
Describe the Production process of insulin
Pre-pro insulin: 109 amino acids Pro insulin: 86 amino acids Insulin:. 51 amino acids
48
Describe the secretion of insulin from the beta cells
*Glucose enters into beta cells via GLUT 2 *Glucose is phosphorylated to glucose-6-phosphate *Glucose 6 phosphate is then oxidized to ATP *ATP acts on the ATP sensitive potassium channels which is usually open by closing it * There is build up of positive charge which depolarizes the membrane *The voltage gated calcium ion channel is activated which will allow for the exocytosis of the insulin vesicles.
49
Name 3 components which are found in an insulin vesicles
Insulin C-peptide Amylin
50
State the functions of Amylin
* delays gastric emptying *Increase glycogenolysis *Inhibits insulin release
51
State the functions of Pancreatic polypeptide
*inhibits gall bladder contractions *Reduce appetite *Controls release of Pancreatic enzymes
52
Which glucose transporter is insulin dependant?
GLUT 4
53
State the organs in which each of the following transporters is found GLUT1-4
GLUT 1: blood brain barrier, heart GLUT 2: Pancreas, Small intestines, liver GLUT 3: Brain, neurons, sperms GLUT 4: Heart, Adipose tissue, skeletal muscle
54
*Stimulates insulin release through feed forward when food is injested *Inhibits glucagon *Reduce gastric emptying What hormone is this?
Incretins Glucose like insulinotropic peptide) Glucose like peptide 1
55
How many amino acids is insulin made up of?
51AA
56
How many amino acids is glucagon made up of?
29
57
Which hormone is produced in 3 locations, hypothalamus,GI tract and Endocrine pancreas?
Somatostatin
58
Describe the pathway of secretion of Cortisol
*Hypothalamus produce Corticotropin releasing hormone *CRH acts on the anterior pituitary gland *Anterior pituitary gland releases ACTH *ACTH stimulates zona fasciculata to release cortisol
59
State the effects of cortisol
* glucose sparing for the brain *Promotes gluconeogenesis * fat oxidation * Increase glucose availability
60
What are the stimuli for cortisol release ?
* Stress * Circadian rhythm
61
A maximum of 500g of glucose can be stored as glycogen.Where is it stored?
Liver: 150g Skeletal muscle:350g
62
How do the beta cells detect the blood glucose concentration?
The enzyme that converts glucose to glucose -6-phosphate has low affinity for glucose GLUCOKINASE ( hexokinase IV) .Its km is 8mmol/L. This means at low physiological concentration ( 2.5-3 mg/dL) little glucose will enter the glycolysis pathway and little ATP will be generated.
63
Describe the insulin receptor
It a dimer made up of 4 subunits. 2 alpha chains on the extracellular and 2 beta chains on the transmembrane
64
Describe the insulin signalling pathway
*Insulin binds on its binding site at the a subunits *Closer of the alpha subunits results in the activation of beta subunits which auto phosphorylated via cross phosphorylation *Insulin receptor kinase is activated. * Insulin receptor substrate (IRS 1) is then attracted to the phosphorylated tyrosine residues and is phosphorylated by insulin receptor kinase *Phosphoinoside 3 kinase ( p13K) binds to the phosphorylated IRS-1 *The active site of p13K moves in close proximity to the membrane where it results in the phosphorylation of phosphatidylinositol-4,5-biphosphate (PIP2) to phosphatidylinositol-3,4,5-triphosphate ( PIP3) *PIP3 travels along the membrane and activates a protein called PIP3 dependant protein kinase (PDK-1) *PDK-1 then activates protein kinase B (AKT)
65
State the 4 functions of AKT in the insulin signalling pathway
*It acts on the AS160 and phosphorylate it resulting in the translocation of the GLUT-4 vesicles to the membrane *Acts on and inhibit the GSK3 which is an inhibitor for glycogenesis,hence glycogenesis is activated *Acts on mTOR which phosphorylated p7056k that carry out protein synthesis *Acts on Fox01 that stimulates PEPCK the key enzyme in gluconeogenesis hence gluconeogenesis is inhibited
66
What is the other name for AKT?
Protein Kinase B
67
Describe the glucagon signalling pathway
Glucagon receptor works via G- stimulatory protein receptor pathway *Glucagon binds to the glucagon receptor. *G stimulatory protein undergoes conformational changes and exchanges Guanosine diphosphate for Guanosine triphosphate. *The subunits of the G-stimulatory protein are activated *The alpha subunit of the G stimulatory protein binds to the Adenyl cyclase on the membrane which converts Adenosine triphosphate (ATP) to cyclic Adenosine Monophosphate (cAMP) *cAMP activates protein kinase A
68
State the functions of Protein Kinase A
*Inhibits glycogenesis by inhibiting glycogen synthase enzyme *Promotes gluconeogenesis by activating PEPCK ( Phosphoenolpyruvate Carboxylase) *Promotes glycogenolysis by activating glycogen phosphorylase enzyme *Inhibits protein synthesis *Inhibits triglyceride synthesis
69
State the 4 main types of oral hypoglycemics
*Biguanides: metformin *Sulfonylureas: Tolbutamide,Glibeclamide, Glipizide *Alpha glucosidase inhibitor: Acarbose *Glitazones (thiazolidinediones): rosiloglitazones, pioglitazone
70
Describe the mechanism of action of Biguanides and it's side effects
Activates AMPK (Adenosine Monophosphate Kinase) which: *Inhibits gluconeogenesis *Decrease intestinal absorption of glucose *Increase insulin sensitivity by increasing glycolysis ( Metformin): first line of treatment SIDE EFFECTS * Weight loss *Abdominal pain,nausea and diarrhoea
71
Describe the mechanism of action of Sulfonylureas and their side effects
Increase Insulin secretion by acting on the ATP sensitive potassium channels * Glibeclamide *Glipizide *Tolbutamide SIDE EFFECTS *Weight gain *Hyperinsulinimia *Hypoglycemia
72
Describe the mechanism of action of glitazones and their side effects
Act on PPAR ( Peroxisome Proliferated Activated receptor ) which is involved in carbohydrates and lipids metabolism. *Increase hepatic glucose uptake by enhancing effectiveness of insulin SIDE EFFECTS *Weight gain *Edema
73
Describe the mechanism of action and side effects of alpha glucosidase inhibitors
*Decrease absorption of carbohydrates SIDE EFFECTS *Diarrhoea and abdominal cramping
74
State the mechanism of action of Gliptins
Gliptins are a novel class of oral anti-diabetic agent that enhance and prolong the physiological actions of incretin hormones by competitively antagonizing the enzyme DPP4
75
Describe the mechanism of action of incretin mimetics
They act like incretins, increase insulin production by feed forward mechanism
75
State the 4 types of insulin
*Rapid acting insulin: aspart, lispro and gluisine *Short acting insulin: regular insulin *intermediate acting insulin: NPH( Neutral Protamine Hagedorm) *Long acting insulin: Glargine
76
State the onset, peak and duration of all different types of insulin
*onset: 3-15min Peak:1hr Duration:4-5hrs *Onset:30min Peak: 2-3 Duration: 5-8hrs *Onset:2-5hrs Peak: Duration:4-12hours *Onsety: 4-6 hours peak; none Duration; 18-24 hours
77
What 2 insulins are the only one that can be administered intravenously? why? How are the others administered and why?
*regular insulin and lispro *They are solutions *The others are administered subcatenously because they are suspensions
78
What is the other name for NPH?
Isophane insulin
79
Describe the composition of the following Actrapid Actraphane
Actrapid: regular insulin Actraphane: regular insulin + NPH
80
State the functions of rapid and short acting insulin
*prevent post prandial hyperglycemia *Decrease risk of late post meal hypoglycemia
81
State the functions of intermediate and long acting insulin
Used to control fasting blood glucose
82
Which type of insulin has no peak?
long acting insulin: Glargine
83
How is a patient with Hypoglycemia treated?
*Give 15-20g of simple carbohydrates by mouth *Give 1mg of Glucagon subcatenously *Give rapid acting insulin intravenously
84
State the 2 components of the insulin secretion curve
Phase 1: Rapid layer burst produced in first 30 minutes phase 2: Gradual longer lasting until blood glucose goes back to normal
85
Describe the insulin secretion curve for Type 2 Diabetes Mellitus
*reduced phase 1 *Delayed peak resulting in post prandial hyperglycemia
86
Describe the insulin secretion curve for Type 1 diabetes mellitus
*no phase1 *low lying and almost staight lying curve
87
In the past, what was the initial insulin made from?
Porcine and beef
88
State the functions of c-peptide
It has a longer half life than insulin and produced in the same amount as insulin hence instead of testing the amount of glucose in the blood we can directly just test for c-peptide
89
What is the half life of insulin?
10 min
90
Apart from the beta cells in pancreas, where is the Hexokinase IV enzyme also found?
Liver
91
How does the control of ATP production control insulin release?
In the secretory pathway of insulin, the ATP molecules have to act on the ATP sensitive potassium channels which results in depolarization of the membrane and finally we end up having the exocytosis of insulin vesicles. Thus, high ATP production results in many insulin vesicles released.
92
What are the effects of insulin?
Promotes glucose uptake in cells Promotes more energy expenditure by the cells Inhibits glucagon Inhibit glycogenolysis Increased formation of triglycerides and protein synthesis Inhibits triglyceride and protein degeneration

SOM 204: GROWTH, REPRODUCTION AND ENDOCRINE GLANDS (35 decks)

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