Diabetes

Question 1

M/c cause of glycosuria

Answer 1

pregnancy

Question 2

Controlled criteria for DM

Answer 2

Glycemic control: - Pre-prandial BG: 80-130 mg/dl. - Post prandial < 180 mg/dl -HbA1C < 7%
2. Body weight. 3. Control BP: (SBP < 130, DBP < 80). 4. Lipid profile: - Total C < 200 mg/dl -TG < 150mg/dl. - LDL- C < 100mg/dl, < 70mg/dl in presence of coronary artery diseases.
- HDL-C > 40 mg/dl in men, > 50 in women (> 45 in both sexes).

Question 3

At what percentage of destruction does the panc have to b in to start experiencing symptoms of DM

Answer 3

90%

Question 4

Most important step in management of a diabetic patient

Answer 4

Urine strip test analysis if it turns from yellow to green it means that it is glucose positive if it turns from white to Violet means it is ketone positive which indicates that this patient is unstable and in a state of diabetic ketoacidosis

Question 5

Which test should be performed for patient presenting with a classical symptoms of hyperglycemia

Answer 5

random blood glucose test

Question 6

Main factor contributing to gestational diabetes mellitus

Answer 6

Human placenta lactogen

Question 7

High risk female for developing gestational diabetes Melitis

Answer 7

1. High risk pregnant female: (MCQ) - factors that increase the risk of GDM are:  Marked obesity.  Previous GDM.  Strong family history of DM.  Old Age > 30 years.  History of macrosomia.
    Glycosuria.

Question 8

Screening of GDM

Answer 8

Initial assessment during the first trimester for high risk patients and if found to be negative should be repeated again during the 24th to 28th weeks gestation

Question 9

Screening method for gdm patients

Answer 9

The Two Step approach consists of a nonfasting oral 50-g glucose load, with a glucose blood measurement 1 hour later(+ve if more than 140)
If the 50-g glucose test is positive, it should be followed by a 100-g, 3-hour oral glucose tolerance test (OGTT)

Diagnostic criteria: - fasting ≥ 95 mg/dl - 1, hour ≥ 180 mg/dl - 2, hours ≥ 155 mg/dl - 3, hours ≥ 140 mg/dl
- ≥ 2 abnormal values to diagnose GDM.

Question 10

TX of GDM

Answer 10

Insulin stopped after delivery and screen after 6 mo
no oral Hypogly cemics

Question 11

recommended physical activity for diabetes

Answer 11

Moderate intensity Exercise 30 minutes 5 days a week

Question 12

drugs to give to diabetes ptn with cardio vascular, kiddney and heart failure

Answer 12

SGLT2
GLP1

Question 13

How do the intermediate and long acting insulin formulations provide their long lasting effects

Answer 13

Intermediate acting mph insulin is covered by PROTAMINE molecules which take a longer time to breakdown
Glargin works by making microcrystalline deposits in the subcutaneous fat so acts as a depot
detemir works by having a fatty acid chain that associates with Albumin prolonging the duration of action
degludec deck works by being a di hexamer That associates into multi di hexamers that take a long time to release insulin into the circulation

Question 14

Types of pre mixed insulin

Answer 14

Premixed human insulin composed of 70% nph and 30% normal insulin premixed analogs which contain either 70% aspart proteomine and 30% aspart or 75% lispro protemen and regular lyspro and the final one is deludec 70% and 30% aspart
Premixed Degludec 70% and 30% liraglutide

Question 15

what is the only non diabetic condition to give insulin to a patient

Answer 15

Certain conditions of hyperkalemia due to renal failure since the administration of insulin with glucose will promote the intracellular passage of potassium

Question 16

How does insulin induce slight ecg changes

Answer 16

Insulin Promotes The passage potassium outside cells which might lead to hypokalemia

Question 17

What is the contraindication of pramlintide

Answer 17

Ptns with diabetic gastroparesis

Question 18

what is the best insulin based treatment regimen for diabetes

Answer 18

Basal bolus regimen

Question 19

Equation for total daily dose of insulin

Answer 19

Weight multiplied by 0.54(type 1 DM)

Question 20

Adjustment for Basal insulin when treating type one diabetes.

Answer 20

Adjustment of basal bolus insulin dose: - 1/2 TDD for bolus insulin dose (÷3 for each meal). - Fix fasting first (controlling fasting blood glucose will control postprandial blood glucose).
- Basal insulin is adjusted to achieve FBG < 130 mg/dl.  130 - 150  increase 2 units.  150 - 170  increase 4 units.  170 - 200  increase 6 units.  > 200  increase 8 units.
Then adjust post prandial blood glucose (to reach ≤ 180) by adjusting bolus insulin increase corresponding dose by 2-4 units every 3-4 days (the doctor said
in the audio that it is 3-7 days, not before 3, better at 5 and best at 7 days).

Question 21

Principle of Tx of type 2 dm

Answer 21

Kiss principle

Question 22

what is the The Somogyi phenomenon

Answer 22

The Somogyi phenomenon: is morning hyperglycemia due to hypoglycemia that happened at night (due to night pp insulin) by the means of stress hormones that rise during the hypoglycemia (cortisol catecholamine glucagon) therefore the
solution is to decrease night dose of insulin or add a snack before bed.
The Dawn phenomenon: is morning hyperglycemia not due to hypoglycemia at night the cause is unclear but the solution is to increase the dose
of night insulin.

Question 23

DKA triad

Answer 23

Uncontrolled hyperglycemia (Diabetic). * Increased total body ketone concentration (ketone).
* Metabolic acidosis (High anion gap) (Acidosis).

Question 24

Alarming symptoms in DKA

Answer 24

GIT symptoms

Question 25

Criteria for severe DKA

Answer 25

Bicarbonate level Less than 10. pH. Less than 7. Anion gap more than 12. affection of consciousness.

Question 26

When is bicarbonate therapy indicated in diabetic ketoacidosis?

Answer 26

When PH levels reach very. low levels like less than 6.9.

Question 27

What are the risks of taking bicarbonate therapy?

Answer 27

It might cause hypokalemia and overshooting and alkalosis.

Question 28

Criteria of resolution of diabetic ketoacidosis.

Answer 28

Both glucose level less than 200 and at least two of the following. bicarbonate level More than 15. Blood PH more than 7.3. Anion gap less than or equal to twelve.

Question 29

DD of DKA

Answer 29

* Other hyperglycemia states: - Stress hyperglycemia. - HHS. * Other ketotic states: - Starvation ketosis. - Alcohol ketosis. * Other high anion gap and metabolic acidosis: (MCQ) - Lactic acidosis. - Uremic acidosis. - Drug induced  salicylates, methanol, paraldehyde and ethylene glycol

Question 30

pathogenesis of hhs

Answer 30

Hyperglycemic Hyperosmolar State (HHS) - It occurs in type 2 diabetics usually elderly patients: due to relative insulin deficiency (Insulin resistance). - HHS is characterized by: o Severe hyperglycemia. o Hyperosmolality. o Severe dehydration. o Absence of significant ketosis. - Which is adequate to prevent lipolysis and subsequent Ketogenesis. (minimal or no Ketoacid). (MCQ) - But inadequate to prevent gluconeogenesis or glycogenolysis. (Severe hyperglycemia therefore severe polyuria → severe dehydration & high osmolarity).

Question 31

Between Dka and edges, which has more cns manifestations.

Answer 31

Because of the severe dehydration, the person will present in.

Question 32

Equation 4 serum osmolarity.

Answer 32

 2 {Serum Na+ (mEq/l)} + glucose (mg/dl) = mOsm/kg. 18

Question 33

Criteria of HHS

Answer 33

1. Hyperglycemia > 600 mg/dl. 2. Effective serum osmolality > 320 mOsm/Kg 3. PH > 7.3 HCO3 > 15 mEq/L. Absent or no ketonemia.

Question 34

Criteria of resolution of hhs

Answer 34

Criteria of resolution: 1. Normal osmolarity. 2. Regain mental status. 3. Blood glucose < 300 mg/dl

Question 35

What is silent MI

Answer 35

ppl with diabetic neuropathy who are unable to feel the pain of mi

Question 36

features of diabetic dyslipidemia

Answer 36

Main features of diabetic dyslipidemia: (MCQ) 1. Increased level of triglycerides more than 150 mg/dl. 2. Low HDL-C less than 40 mg/dl in men and less than 50 mg/dl in women. 3. Normal or increased level of LDL-C more than 100 mg/dl. 4. Increased number of small dense LDL particles. 5. Normal or increased level of cholesterol more than 200 mg/dl

Question 37

typical pattern of dyslipidemia in type 2 diabetes.

Answer 37

Raised triglycerides, low HDL and small dense LDL particles

Question 38

X AND Z syndromes

Answer 38

X syndrome (Metabolic syndrome): 1. Hypertension 2. Obesity 3. Dyslipidemia 4. Insulin resistance (Type 2 DM) Z syndrome: As X syndrome + obstructive Sleep apnea

Question 39

Cause of HTN in type 1 diab ptn

Answer 39

Diabetic nephropathy

Question 40

Cause of HTN in type 2 diab ptn

Answer 40

X(Metabolic syndrome)/Z syndromes

Question 41

anti platelet tx of diab

Answer 41

Use aspirin therapy 75-162 mg/dl as a primary prevention in diabetic patients (type 1&2) at increased cardiovascular risk.(C) - Use aspirin therapy 75-162 mg/dl as a secondary prevention in diabetic patients (type 1&2) with cardiovascular disease.(A) - Aspirin allergy, bleeding tendency, anticoagulant therapy, recent Gl bleeding, under the age of 30 and clinically active hepatic disease are contraindications for aspirin therapy. Clopidogrel (75mg/day) should be used. - May have rapid platelet turnover with diabetic vascular disease; thus, the steady plasma aspirin concentration from the enteric coated preparation theoretically allows for constant suppression of thromboxane synthesis. - May consider clopidogrel 75mg (CAPRIE study) in someone with ASA allergy; was shown to be slightly more effective than ASA in reducing combined risk of stroke, MI, or vascular death in diabetic and nondiabetic subjects.

Question 42

What factors play a role in micro and macro somplications

Answer 42

for macrovascular risk factors . would include not only hyperglycemia, but smoking hypertension, dyslipidemia, obesity, sedentary lifestyle. for microvascular complications , hyperglycemia is the main risk factor.

Question 43

CI of laser photocoagulation

Answer 43

Patients with macular edema. high risk pdr severe cases of npdr

Question 43

Stages of DIabetic retinopathy

Answer 43

1. Mild non proliferative diabetic retinopathy (Mild NPDR): - These changes begin 3 to 5 years after diagnosis in type 1 diabetics. - First signs are microaneurysms with subsequent retinal hemorrhages and hard exudates. - Infarctions of nerve fiber layer, known as soft exudates. - Visual acuity is generally unaffected. 2. Moderate NPDR: - Characterized by microvascular abnormalities such as: 1. Venous beading, venous caliber changes. 2. Increased capillary dilatation and permeability. 3. Severe or very severe NPDR: - Manifested by: * Progressive retinal ischemia. * Extensive hemorrhages, exudates and micro aneurysms. - At 5 years; mild, moderate, and severe NPDR are associated with 15%, 30% and 60% risk of progression to PDR. 4. Proliferative diabetic retinopathy (PDR): Involves: - Neovascularization in the retina "early PDR". - Neovascularization in the vitreous body "High risk PDR" → a. Retinal detachment. b. Retinal hemorrhages. c. Blindness. - Occasionally, new vessels can invade the iris and the anterior chamber, leading to sight threatening closed-angle glaucoma.

Question 44

Risk factors for nephropathy

Answer 44

MAINLY hyper glycemia and glycosylated hemoglobin but other like htn dyslipid smoing genetic

Question 45

at what stage and in what condition do you find kimmelstein wilson nodules>

Answer 45

DIabteic nephro at stage 3(diffuse glumerulosclerosis)

Question 46

at what stage of nephropathy do you find Nephrotic syndrome

Answer 46

diff glomerulosclerosis

Question 47

Stages of CKD

Answer 47

Check diab book pg 62

Question 48

Things that inc albumin exc in urine

Answer 48

Exercise within 24 hours, infection, fever, congestive heart failure, marked hyperglycemia, and marked hypertension may elevate UAE over baseline values.

Question 49

To say ptn had nephropathy he has to have what in the tests of UACR

Answer 49

At least 2 of 3 tests in 3 to 6 mo period be negative

Question 50

What's the prevalence of diabetic nephew and neuropathy?

Answer 50

Diabetic retinopathy is more common in type 1 diabetes patients diabetic nephropathy is common in both types. Diabetic neuropathy symmetrical is common in both, while focal is common in older type 2 patients.

Question 51

Definition of postural hypotention

Answer 51

1. Postural hypotension; defined as: - Drop of systolic BP > 20 or Diastolic > 10 in response to standing (2-3 min). - Manifested clinically by dizziness in response to standing

Question 52

Cardiovascular complications in atomic neuropathy.

Answer 52

Silent myocardial infarctions postural hypotension ecg changes.resting tachycardia

Question 53

Why might diabetic patients not experience symptoms of hypoglycemia?

Answer 53

Attenuated Sampatho adrenal reflex due to autonomic neuropathy.

Question 54

Primary Drugs to be used for patients with neuropathic pain in diabetes.

Answer 54

Pregabalin doluxutine gabapentin

Question 55

Vittiligo associated with type

Answer 55

type 1 diab cuz its autoimmune

Question 56

Diabetic dermoathy pathogenesis

Answer 56

5. Diabetic dermopathy: Multiple small brown macules in the anterior chin of tibia due to microangiopathy rupture of the affected capillaries and deposition of hemosiderin.

Question 57

patho of acanthosis nigricans

Answer 57

Due to excess insulin affecting the cutaneous . cells leading to their hypertrophy.

Question 58

Dermal conditions ass with diab

Answer 58

Acanthosis nigricans diabetic dermopathy NLD(necrobiosis lipodica diabeticorum) vittiligo lipodystrophy xanthelasma bullous diabeticorum

Question 59

How does pentamedine induce hypoglycemia?

Answer 59

Pentamidine stimulates T lymphocytes, which stimulate B cells, to secrete insulin.

Question 60

List the causes of late hypoglycemia

Answer 60

Ediopathic. alcohol related depletes glycogen. Counter regulatory hormone deficiency. IDiopathic immune mediated hypoglycemia. which is classified into three things. First one being insulin receptor agonists. Pentamedine induced. anti insulin antibodies, which form a loose bond with insulin and cause an increase amount of insulin in the circulation which cause hypoglycemia.

Question 61

Explain dumping syndrome

Answer 61

Food reaches the intestine. And before being absorbed, high levels of insulin will be present in the circulation due to the stimulation in the elementary canal. So hypoglycemia will happen.

Question 62

How to diagnose facticious hyperinsulinemia?

Answer 62

High levels of insulin and normal or low levels of seabeptide.

Question 63

Whipples triad and ass with what

Answer 63

FBG LESS THAN 40 Hx of hypoglycemic symptoms immediate improvement after ingestion of glucose. ass with insulinoma

Question 64

Symptoms of insulinoma appear after

Answer 64

missing meal exercise early in the morning

Question 65

Symptoms of insulinoma

Answer 65

Neuroglycopenic symptoms Blurred vision, diplopia, headache, personality changes, mental changes, sweating and petition may not occur due to depletion of counterregulatory hormones. And as. an adaptation of the body to the glycopenia.

Question 66

Causes of hypoglycemic un awareness

Answer 66

Non selective B blockers like propranolol , Insulinoma repeated attacks of hypoglycemia. Autonomic neuropathy.

Question 67

Bed side insulinoma test

Answer 67

Insulin glucose paradox test

Question 68

Tx of insulinoma

Answer 68

Surgery Diet (Injection of glucose at time of meals and frequent complex carbohydrates in between meals) Octreotide streptozocin ODS diazoxide

Question 69

Uses of octreotide

Answer 69

Uses: 1. Acromegaly. 2. Insulinoma. 3. Acute variceal Hge. 4. TSH secreting adenoma. 5. VIPoma. 6. Cushing. 7. Carcinoid tumors.

Question 70

Side eff of octreotide

Answer 70

Decreases heart rate. abdominal cramps, nausea and vomiting. Expensive.`

Question 71

hallmark traid of gout

Answer 71

Hyper uricemia deposition of urate in tissues Attacks of : gouty arth acute and chronic tophaceous gout intercritical period between attacks gouty nephropathy urolithiasis

Question 72

What percentage of ppl with hyperuricemia develop gout

Answer 72

only about 20 %

Question 73

M/C cause of gout

Answer 73

Idiopathic

Question 74

Causes of decreased renal excretion of uric acid

Answer 74

B. Decrease Renal excretion: 1. Intrinsic renal disease ↓ GFR. 2. Renal toxins (lead poisoning). 3. Impaired tubular excretion: a. Metabolic acidosis: lactic acidosis. b. Drugs: thiazides. c. Nephrogenic Diabetic insipidus: vasopressin resistant. d. Salicylate’s poisoning

Question 75

Order of frequency of joint aff in gout

Answer 75

- Ankles  heals  knees  wrist, fingers, elbows (in frequency)

Question 76

Precipitating factors of acute gouty arthritis

Answer 76

* Precipitating factors: 1. Surgery. 2. Trauma. 3. Infections. 4. Alcohol. 5. Exercise. 6. Low temperature. 7. Dietary overindulgence

Question 77

PATHO OF GOUT

Answer 77

* Disruption of subcortical tophus (collection of UA crystal). ↓ * Release of UA crystals into Synovial fluid initial pathogenic event. ↓ * Recognized as foreign & rapidly coated by IgM. ↓ * Phagocytosis of IgM coated UA crystals by leukocytes which release 1st wave bioactive mediators (leukotriene B4 & glycoprotein chemotactic factor). colchicine block 1st wave mediators ↓ * Activate more leukocytes which release 2nd wave mediators (complement, kallikrein, Kinin & Hagman Factor). ↓ * VD & increase capillary permeability. ↓ * Leading to widespread inflammatory reaction  redness, pain, hotness, Swelling & edema

Question 78

TX of acute phase gout

Answer 78

Treatment of acute phase: 1. Joint rest. 2. NSAIDs (1st line). 3. colchicine (2nd line). 4. Steroids (3rd line)  local or Systemic intraarticular.

Question 79

Uricosuric drugs

Answer 79

probencid sulfinpyrazon benzbromarone(mercedes benz bro)

Question 80

Urine alkalizing drugs

Answer 80

NaCo3 Na citrate Acitozolamide

Question 81

Apperance of tophaceous gout

Answer 81

Appear as: 1. White yellowish deposits in external ear. 2. Sub Cutaneous of Finger tips, palms, Soles & around joints. 3. Later stages fusiform on nodular enlargement of Achilles tendon or saccular distention of olecranon bursa.

Question 82

3 CHARACTERS OF TOPHACEOS PAHTO

Answer 82

. Monosodium needles surrounded by mononuclear and giant multinucleated cell reactions and fibroblast formation.

Question 83

How to differentiate tophaceous from? metastatic deposits?

Answer 83

tophaceos Gout has overhanging margins and punched out borders And cortical erosions.

Question 84

What happens in the severe cases of gouty nephroathy?

Answer 84

Moderate proteinuoria. and isothenouia (inabilty to concentrate urine)FIXED LOW SPECIFIC GRAV)

Question 85

Ptho of gouty nephropathy

Answer 85

Deposition of UA crystals in Renal medulla & pyramids leading to mild fibrosis & minimal tubular atrophy So, Renal cortex is not affected by (GFR & renal functions are normal)

Question 86

M/C AND 2ND M/C CAUSE OF TinOSinovitus. and tendinitis

Answer 86

Gout is the 2nd Most common cause of Tendinitis & Tenosynovitis after trauma.

Question 87

What determines the type of lipoprotein?

Answer 87

The apoprotein cap on top of it.

Question 88

Whats the apo in hdl and ldl

Answer 88

HDL apo a1 LDL apo b100

Question 89

Causes of low and high HDL

Answer 89

Causes of low levels: Smoking, obesity (visceral), very low-fat diet, hypertriglyceridemia, drugs; beta blockers, androgenic steroids, androgens progestins (they increase insulin resistance). To increase level of HDL: Life style modification; exercise (decreases weight), stop smoking, drugs; fibrate and Niacin).

Question 90

If there is over prod of APOB what will happen

Answer 90

Familial mixed dyslipidemia.

Question 91

Why does hypothyroidism cause dyslipidemia

Answer 91

Because lipoprotein lipase depends on thyroid hormone.

Question 92

Causes of secondary dyslipidemia

Answer 92

Diabetogenic dyslipidemia, obesity, metabolic syndrome due to insulin resistance. * Alcohol abuse. * Nephrotic syndrome (Hypoalbuminemia decreased lipoprotein formation  increase TG and free cholesterol). * CKD. * Cholestatic liver disease: decreased biliary excretion of cholesterol. - Hypothyroidism: lipoprotein lipase depends on thyroid hormones. Drugs: beta blockers, anabolic steroids, androgens, OCPs, nonselective beta blockers, diuretics, estrogen and ciclosporin. * Bulimia and Anorexia nervosa. * Pregnancy

Question 93

M/C cause of low HDL

Answer 93

DM

Question 94

Central obesity in males and females

Answer 94

More than 94 in males and more than 80 in females

Question 95

When can pth cause bone formation

Answer 95

when given intermittently

Question 96

What is the most common metabolic bone disease

Answer 96

Osteoporosis

Question 97

most common sites for pathologic fractures

Answer 97

vertebral bodies, the distal radius, and the proximal femur

Question 98

Post menopausal osteoporsis affects which type of bone?

Answer 98

Trabecular (like vertebrae)

Question 99

Senile osteoporsis affects which type of bone?e

Answer 99

Trabecular + cortical vert+femur

Question 100

What is a biphasic pattern of bone loss

Answer 100

It is when women experience type 1 and type 2 osteoporosis, postmenopausaly.

Question 101

causes of secondary osteoporosis

Answer 101

Secondary osteoporosis may result from many causes including glucocorticoid excess, male hypogonadism, hyperparathyroidism, hyperthyroidism, malignancy, immobilization, hepatic insufficiency, gastrectomy, rheumatoid arthritis, acromegaly, chronic obstructive pulmonary disease, chronic renal failure, and heparin therapy

Question 102

Effect of cortisol on calcium metabolism

Answer 102

Endogenous or exogenous glucocorticoid excess is a leading cause of premature osteoporosis. Corticosteroids inhibit osteoblastic function, stimulate bone resorption, increase parathyroid hormone secretion, inhibit intestinal calcium absorption, and cause decreased end-organ response to vitamin D

Question 103

What is the chief predictor of osteoporosis

Answer 103

AGE

Question 104

first presentation of osteoporosis

Answer 104

Fracture as its asymptomatic until that occurs

Question 105

What metabolic markers do we use to monitor patients in osteoporosis

Answer 105

OSTEOCALCIN PYRIDINIUM DEOXYPYRIDNIUM HYDROXYPROLINE

Question 106

Why are x rays not reliable in detecting osteoporosis?

Answer 106

Because 30% of the bone needs to be lost in order to be diagnosed and seen as radiolucency

Question 107

Most common cause of incidental finding of osteoporosis on postmenopausal women.

Answer 107

chest x-ray.

Question 108

disadvantages of ct scan for measuring bone densities.

Answer 108

Results are less reproducible more. expensive than other techniques cannot be used for women in childbearing period . High radiation exposure.

Question 109

TEch of choice for bone density measurment

Answer 109

DEXA

Question 110

best bone density measurment tool for young and middle age people

Answer 110

DPA

Question 111

DPA DISADVANTAGES

Answer 111

More expensive less widely available. longer scanning time. falsely elevated results happen in closely situated calcified vessels, compression fractures, degenerative bone diseases.

Question 112

Uses of DPA AND SPA (bones they can scan )

Answer 112

SPA can measure RADIUS ULNA AND HEEL BONES Dpa can measure femur and vertebral bones.

Question 113

types of calcium supplements

Answer 113

Calcium carbonate, which is 40% calcium by weight, but causes more gi symptoms. And calcium citrate, which is 22% calcium by weight, but causes less gi symptoms and is absorbed in patients with achlorohydria

Question 114

daily recommended calcium and VD in ptns of osteo

Answer 114

1500 mg 800IU

Question 115

Effect of exercise (not severe) in elderly women with osteoporosis.

Answer 115

Not significant as not. much bone changes will happen to them, but any reduction in fracture risk is probably. associated with increased muscular strength.

Question 116

How does smoking negate the protective effect of postmenopausal estrogen therapy in osteoporosis ?

Answer 116

Smoking causes increase. metabolism of.estrogen(Estrogen causes an increased production. of vitamin D in the body)