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Endo Flashcards

1
Q

HT eye changes

RB

A

Grade 1: Silver wiring (Increased arteriolar light reflex)
Grade 2: AV nipping (deflection of venule at AV crossing points)
Grade 3: Flame-shaped hemorrhage, cotton wool spot,
Grade 4: Papilledema

Look for LVH, HF

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2
Q

DM eye changes

RB

A

Non-proliferative

  1. Microaneurysm
  2. Dot-blot hemorrhage
  3. Hard exudates

Pre-proliferative

  1. Cotton wool spots
  2. Venous beading
  3. Hemorrhages, IRMA (intraretinal microvascular abnormalities)

Proliferative

  1. NVD/NVE (Neovascularization at disc / elsewhere)
  2. Photocoagulation scars
  3. Vitreous hemorrhage
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3
Q 
MEN 1
(Multiple endocrine neoplasia)
A

Chromo 11 - MEN 1 gene
(aka Wermer syndrome)

  • Pituitary adenoma (Prolactinoma)
  • Pancreas endocrine tumor
  • Parathyroid hyperplasia/adenoma
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4
Q

MEN 2A/2B

Multiple endocrine neoplasia

A 
Chromo 10 - RET gene
2A 
- Parathyroid hyperplasia
- Medullary CA thyroid
- Pheochromocytoma

2B

  • Mucosal neuroma
  • Medullary CA thyroid
  • Pheochromocytoma
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5
Q

Gliptins

A

Dipeptidyl peptidase-4 inhibitor (DPP4 inhibitor)

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6
Q

Whipple’s triad

A
  1. Hypoglycemic Sx
  2. Low plasma glucose (not by H’stix)
  3. Sx relief after increase back plasma glucose

Indicates insulinoma

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7
Q

Insulin types

A
  1. Ultra-short acting (Rapid)
  2. Short-acting (Human insulin)
  3. Intermediate-acting (usu start with this in Type 2)
  4. Long-acting (Basal; usu for type 1)
  5. Pre-mixed
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8
Q

SE of Insulin

A
  1. Hypoglycemia
  2. Weight gain
  3. Lipodystrophy / Lipohypertrophy
    • Routine rotation of injection site recommended
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9
Q

Dose of Insulin for Type 1 DM

A
  • 0.5 unit/kg/day

- Half as basal; half as bolus (further break into tds)

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10
Q

Types of oral DM drugs

x7

A
  1. Biguanide (Metformin)
  2. Sulphonylurea (Gli-)
  3. Meglitinide (-glinide)
  4. Alpha-glucosidase inhibitor (Acarbose)
  5. Thiazolidinediones (-glitazone)
  6. DPP4 inhibitors (-gliptins)
  7. SGLT2 inhibitors (-gliflozins)
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11
Q

Biguanide

A

Metformin

  • Increase insulin sensitivity
  • Decrease hepatic glucose production
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12
Q

Increased risk of DM

A
  1. DM in 1st degree relatives
  2. History of GDM
  3. Age >45
  4. Obesity, HT, dyslipidemia
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13
Q

Metabolic syndrome

A

Cluster of metabolic disorders linked by insulin resistance and asso w/ accelerated atherosclerosis

  1. Glucose intolerance or T2 DM
  2. HT
  3. HyperTG
  4. Decrease HDL
  5. Central obesity (90cm in M; 80cm in F)

Any 3 or more

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14
Q

Sx of Hypoglycemia

A

Adrenergic

  • Palpitation
  • Sweating
  • Tremor

Neuroglycopenic

  • Hunger sensation
  • Restless, anxiety
  • Finger, peri-oral numbness
  • Altered consciousness, drowsiness, coma
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15
Q

Presentation of DKA

A
  1. Lethargy
  2. Dehydration / Hypotension (due to glycosuria)
  3. SOB / Kussmaul breathing (rapid, deep) due to metabolic acidosis
  4. Fruity odor (ketones)
  5. Altered consciousness (due to cerebral edema)
  6. N/V
  7. Abd pain
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16
Q

Presentation of Hyperosmolar non-ketotic coma

A

No N/V, abd pain, Kussmaul breathing

  1. Severe hyperglycemia and dehydration
  2. Depressed sensorium (lack of thirst response: when serum osmolarity >340)
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17
Q

Tx of DKA

A
  1. Replace salt and water deficit - IV NS + K supplement (guided by serum K and renal fx)
  2. Insulin - low dose (5-10 u/h) by continuous IV infusion. ↓Rate when BG <13 mmol/L
  3. Correct acidosis - pH rises with rehydration and insulin. HCO3 infusion if pH <7.1
  4. Identify and treat the cause of DKA
  5. Monitor clinical response, BP/P, urine output; CVP and ECG as indicated
  6. Emergency measures/care of the unconscious patient
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18
Q

H’stix

A

Haemoglucostix

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19
Q

Ix for DKA

A
  1. Plasma glucose
  2. Urine/Serum ketones
  3. Blood gas
  4. Electrolytes
  5. Look for precipitating infections (RS, GI, septicemia, meningitis)
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20
Q

DKA prevent advice

RB

A

Reinforcement of “sick-day” rules
- More freq monitoring of BG during illness
- Check urine or blood for ketones
Marked hyperglycemia require temp adjustment of insulin regimen, if also has ketosis, seek medical help

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21
Q

Causes of HyperPRL

RB

A
  1. Tumor (pressure effect / functional prolactinoma / GH+PRL tumor)
  2. Physiological: preg, breastfeeding
    3 Stress, e.g. venipuncture
  3. Drugs, e.g. methyldopa, chlorpromazine, OCP
  4. Hypothyroidism
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22
Q

Tx of Prolactinoma

RB

A

Medical as primary tx
- Dopamine agonists (Bromocriptine, Cabergoline)

Surgery if drug intolerance/resistance/compliance

Other pit tumors –> transphenodal surgery

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23
Q

Most common causes of HyperCa

RB

A
  1. Primary hyperPTH
  2. HyperCa of malignancy

Others

  1. Excessive Vit D / Ca intake
  2. Hyperthyroidism
  3. Sarcoidosis
  4. Active TB
  5. Familial hypocalciuric hyperCa
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24
Q

Ix for HyperCa

RB

A
  1. Serum albumin
  2. Serum phosphate
  3. ALP
  4. RFT
  5. PTH
  6. 24h urinary Ca excretion

Also,

  • AXR, USG kidneys for stones
  • Bone mineral density assessment
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25
Q

HyperPTH classification

RB

A

Primary
- 80% adenoma; 20% multiple adenoma / hyperplasia; 1% carcinoma

Secondary
- Due to hypoCa in CRF

Tertiary
- Autonomic secretion of PTH after prolonged duration of secondary (e.g. CRF in dialysis)

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26
Q

Ix to localize abnormal parathyroid gland

RB

A

USG, CT, MRI
Radioisotope (Thallium/Sestamibi) scan
Intra-op USG

**Sestamibi scan better than conventional

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27
Q

Indication for surgery for primary hyperPTH

RB

A
  1. Serum total Ca 1mg/dL (0.25mM) above ULN
  2. Hypercalciuria (24h >400mg)
  3. CrCl reduced by >=30%
  4. Renal stone
  5. Osteoporosis
  6. Age <50
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28
Q

Hyperthyroid + neck swelling causes

RB

A
  1. Graves’ disease
  2. Toxic multinodular goiter
  3. Toxic thyroid adenoma
  4. Subacute thyroiditis
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29
Q

Mechanism of anti-thyroid drugs

RB

A

Inhibit TH synthesis - block organification of iodide and coupling of iodotyrosines

PTU in high dose inhibit T4 to T3 conversion

Immunomodulatory effects to reduce thyroid autoAb levels

30
Q

SE of Anti-thyroid drugs
(Thiouracil derivatives (Thionamides): Methimazole, Carbimazole, Propylthiouracil
Lithium - block NaI transporter)
RB

A
  1. Rash (5%)
  2. Agranulocytosis (0.1%)
  3. Cholestatic jaundice, hepatotoxicty (esp PTU), acute arthralgia, ANCA induced vasculitis
31
Q

Graves ophthalmopathy NO SPECS classification

A
  1. No S/S
  2. Only signs (Lid lag, retraction, stares), no Sx
  3. S/S, Soft tissue (swelling, redness)
  4. Proptosis
  5. EOM
  6. Corneal
  7. Sight loss (optic n. atrophy)
32
Q

Sx of Hyperthyroidism

A
  1. LOW
  2. Palpitation
  3. Nervousness
  4. Easy fatiguability
  5. Excessing sweating
  6. Heat intolerance
  7. Hand tremor
  8. Diarrhea
  9. Hair loss
  10. Eye problem

?Amenorrhea

33
Q

Signs of Hyperthyroidism

A
  1. Goiter
  2. Thyrotoxic eye signs (lid lag, lid retraction, periorbital edema, exophthalmos, EOM, corneal involvement, sight loss)
  3. Pretibial myxedema (for Graves)
34
Q

TRAb

A

TSH receptor Ab

Prognostic indicator of outcome of Graves after end of antithyroid drugs

35
Q

Radioisotope thyroid scan in different types of hyperthyroidism

A

Graves –> Diffuse, increase
MNG –> Heterogenous
Toxic adenoma –> Increase focal, rest reduced
TSH-secreting pit adenoma –> Diffuse, increase

Thyroiditis / Iatrogenic / T4 overdose –> Decrease

36
Q

Thyroid surgery Cx

A
  1. Vocal cord dysfunction
    • Damage RLN, external branch of superior laryngeal n.
  2. Hypothyroidism
  3. Bleeding
  4. Tracheomalacia
  5. Thyroid storm
  6. Wound Cx: hypertrophic scar
37
Q

Indication for RAI

A
  1. Thyrotoxic heart disease
  2. Relapse after surgery
  3. CI to surgery
  4. Adult >30y
38
Q

Cx of RAI

A
  1. Hypothyroidism
  2. Fetal risk (avoid preg in 6-12m)
  3. No breastfeeding (excreted in milk)
  4. Thyroid eye disease
  5. Radiation thyroiditis –> thyroid storm
39
Q

Tx of Graves’ ophthalmopathy

A
  1. Make euthyroid
  2. Immunosuppressants (for infiltrative ophthalmopathy)
    • Steroid
    • Cyclosporin A
    • Plasmapheresis
    • Ig
  3. Orbital irradiation
  4. Orbital decompression, eye muscle operation
40
Q

Thyrotoxic periodic paralysis

A
  • In Male
  • HypoK (no net loss, due to IC shifting by insulin)
  • Occur during hyperthyroid (not in euthyroid)
  • Motor involvement (skeletal muscles, seldom RS)
  • Cardiac arrhythmias
  • Tx: Spontaneous recovery, faster if IV K infusion
  • Prevent by low salt diet, appropriate carbohydrate intake, Spironolactone, Propranolol
41
Q

Sx of Hypothyroidism

A
  1. Weight gain
  2. Cold intolerance
  3. Coldness
  4. Constipation
  5. Menstrual irregularities (menorrhagia?)
  6. Muscle cramps
  7. Chest pain

Children: Growth retardation, mental retardation

42
Q

Signs of Hypothyroidism

A
  1. Dry skin
  2. Hoarseness of voice
  3. Slow reflex
  4. Bradycardia
  5. Pallor
43
Q

Half life of TSH / T3 / T4

A

TSH: 1h
T3: 1 day
T4: 1 wk

44
Q

Bone, Stone, Groan, Moan for HyperCa

A

Bone pain
Renal stone
GI: Constipation, abd pain
Psychiatric moans (psychosis, depression)

45
Q

Steroid SE

A

Obesity
- Truncal in distribution, moon face, buffalo hump, supraclavicular fat pads

Skin changes
- Acne, thin skin, excessive bruising, purple striae, pigmentation (Ectopic ACTH or Pituitary Cushing’s)

Proximal myopathy

Psychiatric disturbances in severe cases
- Non-specific, depression, euphoria, frank psychosis

Hirsutism, oligo/amenorrhea in F; impotence in M

Osteoporosis in long term steroid administration

HT, DM

46
Q

Cx of Cushing syndrome

RB

A
  1. CVS: HT, fluid retention
  2. Metabolic: Glucose intolerance, central obesity, HL, hypoK
  3. MSS and skin: thin skin, bruises, striae, proximal muscle weakness, osteoporosis
  4. Immune: Immunosuppression
  5. Psychiatric: Irritability, depression, psychosis
  6. Androgen excess (not in Exogenous): Acne, hirsuitism
  7. For Iatrogenic: AVN, glaucoma, posterior subcapsular cataract
47
Q

Mx of Cushing syndrome

RB

A
  1. Mx concomitant problems: HT, DM, HypoK
  2. Surgery - for cure: Transphenoidal surgery for pit; adrenalectomy for adrenal
  3. Medical: control hypercortisolism before surgery / persist after surgery
    • Metyrapone: Block cortisol synthesis at the final 11β-hydroxylase step; also use to Dx adrenal insufficiency
    • Ketoconazole: Inhibit cortisol and androgen secretion; SE = Hepatotoxicity; actually an anti-fungal
48
Q

Inferior petrosal sinus sampling (IPSS)

A
  • For Dx of Cushing’s disease
  • Pit gland drains to inferior petrosal sinus
  • Increased ACTH compared to the periphery suggests Cushing’s disease
  • Equivocal levels of ACTH indicate ectopic or paraneoplastic Cushing’s Syndrome
  • The sample is usually taken after administration of CRH or DDAVP
49
Q

Classical signs of Acromegaly

RB

A
  1. Prominent supraorbital ridges
  2. Large nose
  3. Prognathism
  4. Deep voice
  5. Oily skin
  6. Thick lips, mal-occlusion, increased interdental separation, macroglossia
  7. Bitemporal hemianopia, optic atrophy/papilledema
  8. Goiter
  9. Large feet, thick heel pads
  10. HT, DM, OA
50
Q

Important Ix for Acromegaly

RB

A
  1. OGTT (measure glucose, GH): GH not suppressed
  2. IGF-1 increased
  3. MRI pituitary
  4. Other ant pit hormones
51
Q

Cx of Acromegaly

RB

A
  1. Facial and skeletal disfigurement
  2. Jaw mal-occlusion and overbite
  3. Arthropathy
  4. Nerve entrapment, CTS
  5. HT, LVH
  6. OSA
  7. DM
  8. Colon polyps, CA
  9. Hypopit secondary to mass efect
  10. Visual defect due to optic chiasm compression

*May have goiter due to viseromegaly; may have hyperthyroidism

52
Q

Mx of Acromegaly

RB

A
  1. Trans-sphenoidal surgery
  2. Medical:
    • Dopamine agonist: Bromocriptine, Cabergoline
    • Somatostatin agonist: Octreotide
    • GH antagonist: Pegvisomant
  3. Primary or adj RT
53
Q

Important Ix for Cushing syndrome

RB

A
  1. 24h free urinary cortisol
  2. Plasma Cortisol and ACTH at 9am and midnight:
    - Loss of diurnal rhythm of cortisol secretion
    - ACTH (low if adrenal cause; high if ACTH-dependent Cushing syndrome)
  3. Screening: 1mg overnight dexamethasone suppression test
  4. Diagnostic of Cushing syndrome: 48h low dose dexamethasone suppression test
  5. High dose dexamethasone suppression test: suppressed = pit-dependent Cushing’s disease
  6. Corticotropin release factor stimulation test:
    Rise in ACTH (>50%) and cortisol (>20%) = pit-dependent Cushing’s disease
  7. MRI pituitary
    MRI/CT adrenals
    Search for underlying malig if ectopic ACTH
  8. Inferior petrosal sinus sampling for ACTH:
    confirm + localization of pit adenoma producing ACTH
54
Q

Important Ix for Graves

RB

A
  1. TFT: serum TSH
  2. Thyroid autoAbs: TSH receptor Ab (TRAb)
  3. Radionuclide scan
    • Diffuse in Graves
    • Patchy inhomogenous for Toxic multinodular goiter
    • Localized increase + other decreased = Toxic adenoma
    • Decrease/no uptake in Subacute thyroiditis
  4. USG: Diffuse enlargement with homogenous echogenicity
55
Q

Cause of secondary HT

RB

A
  1. Renal: Renal a. stenosis, CRF, IgAN
  2. Vascular: Coarctation of aorta
  3. Metabolic: Conn’s syndrome, Cushing’s syndrome, Pheo
  4. Drugs: MC, GC
56
Q

How to form Vanillylmandelic acid (VMA)

A
  • Catecholamines get methylated by COMT in liver and kidney
  • Methylated catecholamines are then deaminated and finally oxidized to vanillylmandelic acid (VMA) which is excreted in urine
  • COMT = Catecholamine-o-methyl transferase
57
Q

Pheochromocytoma facts

A
  • Arises from chromaffin cell of adrenal medulla
  • 20% extra-adrenal; 24% familial (MEN2, neurofibromatosis)
  • Up to 36% malignant
  • Extra-adrenal tumors tend to produce NA whereas adrenal tumors usually produce both NA + A
58
Q

Presentation of Pheochromocytoma

A
  1. Due to excess catecholamine secretion
    - HT, headache, palpitation, pallor, anxiety, tremor, dizziness
    - Hypermetabolism, sweating, LOW, glucose intolerance, angina
  2. Due to Cx
    - LVF, CVA, MI, encephalopathy
59
Q

Dx of Pheochromocytoma

A
  1. Urinary VMA (Vanillylmandelic acid)
  2. Urinary catecholamines and their metabolites (Metanephrine and normetanephrine)
    * *Beware of drug and dietary interference (e.g. BB, methyldopa)
  3. Plasma catecholamines if available
  4. Localization by imaging

4a. CT/MRI
- Contrast ingestion may induce a pressor crisis and patients should be prepared with complete adrenoceptor blockade

4b. Meta-iodo-benzyl guanidine (MIBG) scan
- Taken up by chromaffin tissue
- Labelled with radioactive iodine (I-123) and results in adrenomedullary images 24-48h after injection

60
Q

Tx of Pheochromocytoma

A
  1. Surgery
  2. Full α+β blockade before surgery or any procedures to prevent crisis
  3. Initially blockade with Phenoxybenzamine (Nonselective α-blocker) , then β-blockade with Propranolol
  4. Important to institute α-blockade first
    - If β-blocker administered first, vasoconstriction due to unopposed α-adrenoceptor activity may occur and exacerbate HT
61
Q

Distribution of fat measurement

A

Assessed clinically by Waist:Hip ratio or Waist circumference

  • Upper body obesity: WHR >= 0.95 in M // >=0.8 in F
  • Waist circumference (as a measure of central obesity): >=90cm in M // >=80cm in F
62
Q

Secondary causes of obesity

A
  1. Hypothyroidism
  2. Cushing syndrome
  3. Hypogonadism in M
  4. PCOS in F
  5. GH deficiency
  6. Hypothalamic tumors
63
Q

Mx of severe hyperCa

A
  1. Fluid replacement
    - NS
    - Excrete Ca by inhibition of Na reabsorption @ PT and Loop
    - Monitor fluid and electrolyte balance
  2. Frusemide
    - To increase urinary Ca excretion
    - Only give after adequate fluid hydration
  3. Bisphosphonates
    - ↓Bone resorption
    - IV preparations potent and rapid onset
    - Currently the most commonly used tx
  4. Calcitonin
    - ↓Bone resorption
    - Fall in Ca is small
    - Lack of severe SE
    - Rapid onset of action
  5. Corticosteroids
    - ↓Bone turnover
    - Useful in patients with myeloma, leukemia, lymphoma, sarcoidosis, vitamin D intoxication
64
Q

Presentation of HypoCa

A
  • Paresthesia, circumoral嘴邊的numbness
  • Tetany (Trousseau’s sign, Chvostek’s sign)
  • Hyperventilation
  • Convulsion
  • Laryngeal spasm
  • ECG: prolonged QT interval
65
Q

Tx of HypoCa

A
  • Severe: IV Ca gluconate by infusion

- Mild: Oral replacement of Ca; 1,25 (OH)2D3

66
Q

HbA1c FP, FN

A

FP:

  1. CKD (glycation↑)
  2. Iron deficiency (erythropoiesis↓)
  3. Assay issue (bilirubin)

FN:

  1. ↓life span (blood loss, hemolysis, hypersplenism)
  2. Blood transfusion
67
Q

Somogyi and Dawn phenomenon

A

Somogyi

  • Rebound hyperglycemia before meals or during night as hypoglycemia stimulates release of counter-acting hormones; sometimes overcompensation causing hyperglycemia
  • Good HbA1c, high FG despite increase dose of morning basal insulin

Dawn

  • Early morning hyperglycemia due to surge of counteracting hormones during sleep as insulin wanes during night, between 4 to 7am
  • Physiological
Differentiate by
Differentiation
- 2am h’stix
- Continuous glucose monitoring system
- Hypoglycemia at 2am --> Somogyi phenomenon

Mx
Somogyi –> reduce bedtime coverage (adequate carbohydrate intake, snack before night)

Dawn –> increased bedtime coverage (NPH or long acting; later in evening or at bedtime)

68
Q

Precipitating factors for DKA/HHS

A
  • Infection, OT, trauma, severe emotional stress
  • MI, Stroke (esp. in elderly)
  • Drug e.g. steroid
69
Q

Anti-TPO Abs

wiki

A

Anti-thyroid peroxidase Abs

In 90% of Hashimoto’s thyroiditis, 75% of Graves’ disease and 10-20% of nodular goitre or thyroid carcinoma

70
Q

Other causes of Hyperprolactinemia

non-stressed PRL usu <3x normal

A

*Pain when sticking needle will increase PRL level; leave it for 30 mins to take blood to get the basal PRL level

Physiological (Pregnancy, Lactation)
Pathological
1. Lesions (e.g. tumors) involving hypothalamus or pituitary stalk
2. Estrogen containing medications (E can stimulate PRL producing cells)
3. Drug affecting central dopaminergic regulation (anti-psychotic drugs, anti-emetics, alpha methyldopa, H2 antagonists)
4. Idiopathic

Others

  1. Hypothyroidism: ↑TRH (Thyrotropin releasing hormone)
  2. Renal failure: Impaired dopamine action, reduced PRL clearance
  3. Chest injury
71
Q

Dx of GH producing tumors

A
  1. ↑Serum IGF-1

2. Non-suppressible Serum GH during OGTT

72
Q

Dx of Prolactinomas

A
  • Prolactin; usually >10x normal

- Tumor shrinkage by >50% in 90% patients when treated with dopamine agonists

Medicine (9 decks)

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