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Internal Medicine pt.1 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Where is insulin secreted from?

A
  • b-cells of islets of langerhans

- secreted as pro insulin & splits into insulin & C-peptide

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2
Q

What is the function of insulin?

A
  • increases uptake & utilization of glucose
  • stimulates glycogenesis
  • inhibits gluconeogenesis
  • stimulates lipogenesis
  • inhibits lipolysis
  • inhibits ketogenesis
  • anabolic
  • intracellular shift -> K
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3
Q

What stimulates the secretion of insulin?

A
  • glucose
  • aminoacids
  • sulphonylurea
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4
Q

What will inhibit the secretion of insulin?

A
  • hypoglycemia
  • hypokalemia
  • somatostatin
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5
Q

What are the effects of insulin deficiency on the body?

A

hyperglycemia

  • decreased uptake & utilization of glucose
  • decreased glycogenesis & lipogenesis
  • increased glycogenolysis & gluconeogenesis
  • increased lipolysis
  • increased ketogenesis
  • catabolism
  • loss of K
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6
Q

What is the definition of diabetes mellitus?

A

disturbance of carbohydrate metabolism due to insulin deficiency or resistance or both
leading to hyperglycemia & glucosuria with secondary disturbance of protein & fat metabolism

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7
Q

What is the classification of diabetes mellitus?

A

PRIMARY

  • type I: insulin-dependent DM
  • type II: insulin-independent NIDDM

SECONDARY

  • pancreatic diseases (cystic fibrosis, hemochromatosis, pancreatitis)
  • endocrinal diseases (acromegaly, cushing’s, pheochromocytoma, thyrotoxicosis)
  • chronic liver failure
  • drugs (corticosteroids, contraceptive pills, thiazide)
  • genetic diseases (DIDMOAD, down, myotonia atrophica)
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8
Q

What is the cause of type I DM?

A

damage of b-cell in islets of langerhans

  • genetic: HLA dr3-dr4
  • infection: coxsackie B, rubella, mumps
  • immunological mechanisms: islet cell antibodies ICA, antiGAD (glutamic acid decarboxylase), insulin autoantibodies IAA
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9
Q

What are the causes of type II DM?

A
  • insulin resistance at receptor or post-receptor level

- dysinsulinogenesis

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10
Q

What are the phases of type II DM?

A
  • early: high insulin levels & loss pulsatile insulin secretion
  • late: decrease in insulin levels & loss of 1st phase insulin secretion
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11
Q

How does a patient with diabetes mellitus present?

A
  • polyuria
  • polydipsia (thirsty)
  • polyphagia (hungry)
  • pruritis
  • parathesia & premature loosening of the teeth
  • repeated infection
  • complications
  • diabetic coma
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12
Q

What investigations are done for diagnosis of diabetes?

A 
1- plasma glucose 
2- urine analysis
3- investigate for cause (only if secondary diabetes is suspected) 
4- investigate for complications 
5- monitor treatment
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13
Q

How is the plasma glucose measured & what are the normal results?

A
  • fasting glucose: normal from 70-99mg
  • 2 hours post-prandial: <140mg
  • oral glucose tolerance OGTT: <200mg
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14
Q

When is a diabetes diagnosis confirmed after measuring the plasma glucose?

A
  • fasting glucose: 126 or more
  • 2 hours post-prandial: 200 or more
  • OGTT: >200 in 2 readings
  • symptoms of diabetes + random plasma glucose of 200 or more
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15
Q

What is the most important marker for diagnosis of DM?

A

Hemoglobin A1-C (HAIC): normal is < 5.7

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16
Q

How should the treatment of DM be monitored?

A
  • home blood glucose monitoring (HBGM)
  • HA1c (glycosylated hemoglobin): formed by linkage of glucose to B-chain of HbA (used to estimate control for preceding 8-12 weeks)
  • fructosamine: glycosylated plasma protein (control over past 2 weeks)
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17
Q

What is the classification of findings of HA1C?

A
  • normal: 5 - 5.6 (<5.7)
  • prediabetes: 5.7 - 6.4
  • diabetes: 6.5 & above
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18
Q

What are the causes of mellituria (sugar in urine)?

A
  • DM

- renal glycosuria: due to low renal threshold for glucose (Dentoni-fanconi syndrome & pregnancy)

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19
Q

How should diabetes be treated?

A 
1- dietetic control 
2- general measures 
3- oral hypoglycemia drugs 
4- insulin 
5- new lines of treatment 
6- ttt of complications 
- ttt of the cause is secondary
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20
Q

What are the proportions of food elements in dietetic control?

A
  • CARBS -> 50% of total caloric intake
  • FATS -> 30%
  • PROTEINS -> 20%
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21
Q

What are the values of weight reduction?

A
  • decrease hepatic glucose production
  • decrease insulin resistance
  • improve b-cell function
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22
Q

What is the exercise guide for diabetic FITness?

A

Frequency -> 3x to 4x a week
Intensity -> 60-80% of maximal heart rate
Time -> 20-30mins

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23
Q

What is the classification of oral hypoglycemic drugs?

A 
SULPHONYLUREA
old generation (long half-life -> high risk of hypoglycemia) 
- tolbutamide 
- acetohexamide 
- chloropropamide
new generation (short half-life -> less hypoglycemia)
- glibenclamide 
- glipizide 
- gliclazide 
- glimepiride

BIGUANIDES
- metformin

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24
Q

what are the adverse effects sulphonylureas?

A
  • hypoglycemia: most severe with chloropropamide
  • hyponatraemia with chloropropamide
  • skin reactions: alcoholic flush, dermatitis
  • hepatitis & cholestatic jaundice
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25
Q

What drugs affect the function of sulphonyureas?

A
  • INCREASED BY: NSAIDS, sulfonamides, chloramphenicol

- DECREASED BY: corticosteroids, estrogen, rifampicin

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26
Q

What is the mechanism of action of (biguaninde) metformin?

A
  • decrease plasma glucose & gluconeogenesis
  • decrease intestinal absorption of glucose
  • increase sensitivity of insulin receptor
  • decrease body weight through its anorexogenic
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27
Q

What is the recommended dose for metformin (glucophage)?

A

start with 500mg & increase up tp 2500mg

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28
Q

What are the side effects of metformin?

A
  • nausea
  • vomiting
  • diarrhea
  • B12 malabsorption
  • anorexia
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29
Q

What are the indications for insulin therapy?

A
  • all IDDM patients (type I)
  • NIDDM (type II) if not responding to diet & oral drugs
  • diabetic ketoacidosis
  • diabetes during pregnancy
  • complicated diabetes
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30
Q

What are the types of insulin?

A

rapid-acting

  • onset: 10-15mins
  • peak: 60-90mins
  • duration: 4-5 hours

short-acting

  • onset: 0.5-1 hour
  • peak: 2-4 hours
  • duration: 5-8 hours

intermediate-acting

  • onset: 1-3 hours
  • peak: 5-8 hours
  • duration: up to 18 hours

extended long-acting

  • onset: 90 minutes
  • no peak
  • duration: 24 hours

premixed
- taken twice a day: once with breakfast & once before supper

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31
Q

What are the methods of insulin administration?

A

CONVENTIONAL INSULIN THERAPY

  • 2 SC injections -> 2/3rd before breakfast & 1/3 before dinner
  • each dose 30% short acting & 70% intermediate acting

MULTIPLE SUBCUTANEOUS INSULIN INJECTION (MSII)

  • 40% intermediate insulin AT BEDTIME
  • 60% regular insulin before the 3 main meals (20% for each meal)

CONTINUOUS SUBCUTANEOUS INSULIN INFUSION (CSII)

  • 40% of total dose is given basally & remainder (60%) is given as preprandial boluses
  • risk of hypoglycemia & hyperglycemia
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32
Q

What are the side effects of insulin administration?

A
  • hypoglycemia
  • hypersensitivity
  • insulin resistance
  • insulin lipodystrophy (atrophy or displacement) at site of injection
  • Somogi phenomenon
  • Dawn phenomenon
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33
Q

How can we differentiate between Somogi & Dawn phenomenas?

A

measure glucose at midnight

  • Somogi -> hypoglycemia THEN hyperglycemia
  • Dawn -> hyperglycemia
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34
Q

What is the difference between Somogi & Dawn phenomenas?

A
  • Somogi -> overdose of insulin given at night (treat by decreasing evening insulin)
  • Dawn -> night dose of insulin was not enough
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35
Q

What is the honeymoon phase & what should be done during this phase?

A

decrease in insulin requirement in IDDM due to TEMPORARY islet cell function

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36
Q

What are the acute complications of diabetes?

A
  • diabetic ketoacidosis DKA
  • hypoglycemia
  • hyperglycemic-hyperosmolar non ketonic coma HHNC
  • lactic acidosis
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37
Q

What are the predisposing factors for DKA?

A 
1- inadequate insulin administration in type I 
2- increase in insulin requirement 
- infections 
- MI
- emotional stress 
- excess fat intake 
- starvation 
- endocrinal disorders 
- pregnancy & labour 
- trauma, operation, burn, & shock 
- non cause (25%)
38
Q

What is the pathogenesis of DKA?

A

1- severe insulin deficiency
2- utilization of fats for energy
3- increase glycerol & FFA
4- formation of ketone bodies (acetone, aceto-acetic acid, B-hydroxy-buteric acid)

39
Q

The increase of ketone bodies will lead to?

A
  • metabolism acidosis -> air hunger & acetone odor
  • hyperglycemia -> glucosuria -> polyuria & dehydration
  • electrolyte imbalance -> decreased level of consciousness
40
Q

What is the clinical picture of DKA?

A

POLYURIA

  • polydipsia
  • dehydration -> weakness, tachycardia, hypothermia

KUSSMAUL RESPIRATION shallow rapid breathing

GIT

  • acetone odor
  • anorexia nausea, vomiting, & hematemesis
  • iléus -> abdominal distention, constipation & gastric dilatation due to hypokalemia
  • severe abdominal pain due to ketonemia

CNS

  • hypotonia & hyporeflexia due to hypokalemia
  • coma due to -> ketone bodies, dehydration, acidosis, & electrolyte disturbance
41
Q

What will be found on investigation of DKA?

A
  • plasma glucose -> higher than 300 (hyperglycemia)
  • urinalysis -> glucosuria, ketonuria, ketonemia
  • ABG -> decrease in HCO3 <10 with pH <7.3
  • electrolytes -> hyperkalemia (extracellular shift)
    if hypokalemic from the start -> patient is severely dehydrated & need aggressive K treatment
  • increase in PCV due to marked dehydration
42
Q

How should DKA be treated?

A 
1- preventive 
2- curative 
- fluid replacement 
- insulin treatment 
- electrolyte correction 
- sodium bicarb 
- treat cause
43
Q

What is the adequate fluid replacement therapy in case of DKA?

A
  • up to 8 liters per day
  • 1L in first 1/2h -> after 1 hr 1L -> after 2h 1L -> after 3h 1L -> after 4h 1L = 5L in half the day
  • normal saline is used until blood glucose is <200mg THEN changed to dextrose - saline
44
Q

How should insulin be given in treatment of DKA?

A

IV infusion insulin

  • start with 0.1 u/kg/h -> MAX decrease blood glucose 50-100mg/h (could cause brain edema if more)
  • continue until glucose conc. <200mg
45
Q

What is the normal potassium level?

A

3.5 - 5.5

46
Q

How do we correct electrolyte disturbances in DKA?

A
  • if K is more than normal (5.5) -> do nothing because insulin will bring it down
  • if K is normal (3.5 - 5.5) -> give K with insulin
  • if K is <3.5 -> DO NOT START INSULIN & give potassium 40mmol/L of saline
47
Q

When should bicarb be given in DKA?

A

when

  • HCO3 is <10
  • pH is <7.1
48
Q

What are the complications of DKA?

A
  • Rhinocerebral mucormycosis -> fatal within 1 week -> treat with amphotericin + necrotic tissue removal
  • shock -> due to severe dehydration
  • vascular thrombosis -> due to severe dehydration
  • pulmonary edema -> due to aggressive fluid therapy -> give furesumide
  • cerebral edema -> rapid decrease of glucose levels -> movement of water into intracellular space
49
Q

What are the manifestations of brain edema & how are they treated?

A
  • increased intracranial tension -> papilloedema, opthalmoplegia
  • confusion & recurrence of coma

treat by mannitol or dexamethasone

50
Q

how is hypoglycemic coma treated?

A

IV glucose

51
Q

hyperglycemic-hyperosmolar non-ketotic coma is common in which patients?

A

old diabetic patients

52
Q

What is the pathogenesis of HHNC?

A

1- low level of insulin that prevents lipolysis & ketosis BUT NOT enough to prevent hyperglycemia (>800mg)
2- osmotic diuresis
3- severe dehydration

53
Q

What are the predisposing factors of HHNC?

A
  • conditions increasing insulin requirement

- drugs inhibiting insulin secretion -> steroids, K-wasting diuretics, diazoxide, & phenytoin

54
Q

How should HHNC be treated?

A

1- half tonic saline
2- lower rate of insulin infusion 3u/h -> because there is a higher risk of cerebral edema
3- low dose s.c heparin -> prevent thrombosis damage from dehydration

55
Q

What will cause lactic acidosis is diabetic patients?

A

patients receiving BIGUANIDES -> anaerobic glycolysis -> accumulation of lactic acid in excess -> coma

GIVE A LARGE AMOUNT OF HCO3

56
Q

What are the chronic complications of diabetes?

A

1- neurological complications -> cerebral, spinal cord, neuropathy
2- cardiovascular complications -> atherosclerosis, microangiopathy, cardiomyopathy, increase HTN
3- respiratory complication -> infections (TB), kussmaul breathing, acetone odor
4- gastro-intestinal complications
5- urinary complications -> UTI, diabetic nephropathy
6- genital complications -> impotence, loss of testicular sensations, pruritis vulvae, vaginalis moniliasis, menorrhagia, sterility
7- ocular complications -> infections, error of refraction, diabetic cataract, rubeosis iridis, diabetic retinopathy
8- skin complications

57
Q

What are the neurological complications?

A

Cerebral

  • coma
  • cerebral atherosclerosis & thrombosis
  • rhino-cerebral mucor mycosis

Spinal

  • posterior column affection -> diabetic pseudotabes
  • pyramidal tract affection -> diabetic lateral sclerosis

Neuropathy

  • sensory
  • motor
  • autonomic
58
Q

What are the symptoms of sensory neuropathy?

A

peripheral symmetrical paraesthesia or hyperesthesia with nocturnal intensification

  • starts in the feet -> glove & stocking hypoesthesia
  • deep sensations are lost early
59
Q

what are the complications of sensory neuropathy?

A
  • neuropathic skin ulcers

- neuropathic (Charcat’s) joint

60
Q

What are the types of motor neuropathy?

A
  • mononeuropathy -> isolated motor nerve paralysis
  • mononeuropathy multiplex -> isolated unrelated multiple motor nerve paralysis
  • polyneuropathy -> bilateral symmetrical distal motor weakness with sensory loss
61
Q

What is the pathogenesis of diabetic neuropathy?

A
  • ischemia secondary to narrowing to vasa nervosum -> mononeuropathy & mono multiplex
  • accumulation of sorbitol -> polyneuropathy
62
Q

What are the symptoms of autonomic neuropathy in the genito-urinary system?

A

parasympathetic is affected first -> sympathetic takes the upper hand in the beginning

EARLY (parasympathetic affection)
- straining, dribbling, reduction in the force of stream
- failure of erection
LATE (both affected)
- bladder distention with overflow incontinence
- failure of ejaculation

63
Q

What are the symptoms of autonomic neuropathy in the cardiovascular system?

A
  • persistent sinus tachycardia
  • postural hypotension -> due to pooling of blood
  • painless MI
64
Q

What are the symptoms of autonomic neuropathy in the gastro-intestinal tract?

A
  • gastroparesis diabeticorum -> slow emptying, distention, vomiting
  • intermittent bouts of diarrhea alternating with constipation
  • fecal incontinence
65
Q

What are the effects of autonomic neuropathy on sweating?

A
  • initially excessive nocturnal sweating
  • gustatory sweating -> during eating
  • later -> diminished sweating in the lower limb (anhydrous)
66
Q

What are the vasomotor disturbances that occur due to autonomic neuropathy?

A
  • edema of the feet & legs
  • increase temperature in lower extremities -> burning hot feet at night
  • unawareness of hypoglycemia
67
Q

How should painful neuropathies be treated?

A

1- NSAIDS or tramadol
2- phenytoin or carbamazepine, gabapentin, pregabalin
3- TCA
4- topical Capsaicin (VIX)

68
Q

What are the special features of atherosclerosis in diabetes?

A
  • more extensive
  • occurs earlier
  • equal sex incidence
  • > peripheral vascular disease
  • > CAD & stroke (CVA)
69
Q

What are the effects of microangiopathy?

A
  • vasa nervosa -> neuropathy
  • glomeruli -> nephropathy
  • retinal vessels -> retinopathy
70
Q

How should hypertension be controlled incase of diabetic patients?

A

ACEs & ARBs

contraindications

  • non selective BB -> masks hypoglycemia manifestations
  • thiazides -> worsens blood sugar control
  • methyl dopa & guanethidine -> worsens postural hypotension
71
Q

What are the chronic GI complications of diabetes?

A
  • tongue -> dry, beefy, oral moniliasis (red & inflamed)
  • teeth -> loose, dental caries
  • gastroparesis diabeticorum
  • gallbladder stones & chronic cholecystitis
  • nausea, vomiting, & hematemesis
  • nocturnal diarrhea & constipation
  • NAFLD
72
Q

What are the stages of diabetic nephropathy?

A
  • stage I -> hypertrophy & hyper filtration (normally GFR is 125)
  • stage II -> hyper filtration & microalbuminuria (on exercise) -> 30-300mg/24hrs
  • stage III -> hyperfiltration & constant microalbuminuria
  • stage IV -> proteinuria > 300mg/24hrs & decrease GFR
  • stage V -> end stage RF
73
Q

How is diabetic nephropathy delayed?

A
  • diabetic control -> reverses microalbuminuria
  • hypertension control -> MAX 130/80 but the lower the better -> ACE inhibitors
  • low protein diet
74
Q

What are the effects of pregnancy on diabetes?

A
  • insulin resistance
  • decreased renal threshold for glucose
  • increased incidence of ketosis & acceleration of diabetic complications
75
Q

What are the effects of diabetes on pregnancy?

A

ON FETUS

  • neonatal hypoglycemia
  • large birth weight
  • congenital anomalies
  • increased incidence of abortion, premature delivery & neonatal death

ON MOTHER

  • increase incidence of toxemia, hydramnios, & placental dysfunction
  • post partum hemorrhage
  • puerperal sepsis
76
Q

What are the types of errors of refractions due to diabetes?

A
  • hyperglycemia -> myopia

- hypoglycemia -> hypermetropia

77
Q

What are the stages of diabetic retinopathy?

A

1- sclerosis of retinal arteries
2- microaneurysms
3- deep round hemorrhages & yellowish-white waxy exudates
4- vitreous hemorrhages & fibrous tissue formation (retinitis proliferans) -> obscure vision & subsequent shrinkage of fibrous tissue -> retinal traction & detachment

78
Q

What are the primary skin complications due to diabetes?

A
  • diabetic dermopathy (shin spots)
  • bullosis diabeticorum
  • necrobiosis lipoidica diabeticorum
  • acanthuses nigerians
  • eruptive xanthomas
  • insulin lipodystrophy
  • scleroderma
  • lipohypertrophy
79
Q

How should we screen for gestational diabetes?

A
  • any pregnant female with diabetes risk factors -> screen at first prenatal visit
  • if pregnant female has no risk factors -> screen on the 24-28 week using 2h OGTT (75g load)
80
Q

What is the diagnostic criteria for gestational diabetes?

A
  • fasting blood glucose ≥92 mg/dL
  • 1hr post-glucose challenge ≥180mg/dL
  • 2hr ≥153mg/dL
81
Q

How should gestational diabetes be treated?

A

PREPREGNANCY PLANNING
- HBA1c must be normalized

DURING PREGNANCY

  • keep FBG 60 - 110
  • check glycosylated Hb every month

DURING LABOUR
- maternal blood glucose should be kept within 80 - 100mg

82
Q

What are the causes of hypoglycemia?

A

FASTING HYPOGLYCEMIA

  • decrease glucose production
  • increase glucose utilization

POSTPRANDIAL HYPOGLYCEMIA

  • hyperalimentation: after gastrectomy -> brisk glucose absorption -> excessive insulin release -> hypoglycemia after 2 - 3 hrs
  • idiopathic reactive hypoglycemia: hypoglycemia after 3-5 hrs
83
Q

What are the causes of decreased glucose production?

A
  • hormone deficiency -> hypopituitarism, adrenal insufficiency, hypothyroidism
  • enzyme deficiency -> decrease in enzymes responsible to breakdown of glycogen
  • substrate deficiency
  • acute liver disease -> severe hepatitis
84
Q

What are the causes of increased glucose utilization?

A
  • increased insulin: insulinoma, exogenous insulin, sulphonylurea
  • increase insulin life growth factor: fibroma, sarcoma, hepatoma
  • decreased enzymes of fat oxidation: decreased carnitine enzyme -> all tissue becomes obligate consumers like the brain
85
Q

What is the clinical picture of hypoglycemia?

A

ADRENERGIC MANIFESTATIONS

  • anxiety
  • sweating
  • tremors
  • palpitations
  • weakness
  • tingling of mouth
  • hunger

BRAIN

  • headache
  • mental dullness, confusion, & visual disturbance
  • convulsions
  • coma
86
Q

How can we diagnose fasting hypoglycemia?

A

Confirming of fasting hypoglycemia

  • fasting for 16 - 72 hrs -> estimate plasma glucose & insulin every 6 hours
  • ratio of insulin/plasma glucose should always be less than 0.4 in normal people

Determining the cause of FH

  • abdominal US or CT
  • endocrine or enzyme assay
87
Q

How should fasting hypoglycemia be treated?

A
  • adrenergic reaction without CNS abnormalities -> oral carbohydrates
  • if coma or confusion -> IV glucose 25 - 50 as a bolus -> constant infusion until patient is able to eat

treat the cause

88
Q

How should post prandial hypoglycemia be treated?

A

1- diet -> small frequent meals with limited amounts of carbs
2- drugs -> propanthelin & phenytoin
3- surgery -> for refractory cases

89
Q

What is the criteria for diagnosis of metabolic syndrome?

A

1- central obesity -> in saudi ≥102 in males & ≥84 in females
2- any two of the following
-> raised triglycerides >150 mg/dL
-> reduced HDL cholesterol < 40 mg/dL in males & < 50 mg/dL in females
-> systolic BP > 130 or diastolic BP > 85
-> raised FPG > 100mg/dL
OR TREATMENT OF ANY

90
Q

What is the mechanism of action of metformin & its contraindications?

A

suppresses hepatic glucose output

contraindicated in:

  • renal compromise (CR > 1.4 in women & 1.5 in men)
  • CHF requiring treatment
  • increased lactic acidosis
91
Q

What is the mechanism of action of sulfonylureas & its precautions?

A

increases pancreatic secretion of insulin (gli-)

leads to

  • weight gain
  • hypoglycemia
92
Q

What is the mechanism of action of acarbose & its precautions?

A

delays glucose absorptions by inhibition of pancreatic a-amylase & intestinal a-glucoside

causes GI

  • flatulence
  • cramps
  • diarrhea

Internal Medicine pt.1 (33 decks)

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