Endocrinology Flashcards

Question

How does the Synthesis of Nitric oxide occurs ??

Answer 1

aka Endothelium derived Relaxation factor - formed from L-Arginine & O2 by Nitric oxide synthase (NOS) - Has a very short 1/2-life (seconds), inactivated by O2 free radicles

Answer 2

Acts on Guanylate cyclase leading to raised intracellular cGMP => decreases Ca2+ levels - Vasodilation (mainly Venodilation) - INHIBITS Platelet aggregation

Answer 3

- Reduces NO production is implicated in Hypertrophic Pyloric S - Lack of NO: Atherosclerosis - In Sepsis, increased NO levels: Septic Shock - Organic Nitrates (metabolism produced NO) is widely used to treat CVS diseases (eg Angina, HF) - Sildenafil

Answer 4

Anterior Pituitary (Somatotrophs comprise 50% of cells of anterior pituitary) - Postnatal growth & devt. - Actions on Protein, Carbohydrate & Fat metabolism ( increased lipolysis & gluconeogenesis)

Answer 5

Acts on Transmemb. receptor for growth factor - Binds to this receptor => Receptor Dimerization - Acts directly on tissues & also Indirectly via IGF-1

Answer 6

primarily by Liver

Answer 7

INCREASED Secretion - GHRH (released in pulses by Hypothalamus) - Fasting. - Exercise. - Sleep (particularly Delta sleep) DECREASED Secretion - Glucose - Somatostatin (itself is increased by somatomedins, circulating IGF-1 & 2)

Answer 8

Z Glomerulosa : MCs mainly Aldosterone Z Fasciculata : GCs mainly Cortisol Z Reticularis : Sex steroids; mainly Dehydroepiandrosterone (DHEA)

Answer 9

Enzyme released by JG cells in response to REDUCED Renal perfusion - Renin HYDROLYSES Angiotensinogen ==> A-1

Answer 10

Factors (+) Renin - Hypotension - Hypo Na+ - Sympathetic nerve stimulation - Catecholines - Erect posture Factors that reduce Renin - Drugs: Beta-blockers, NSAIDs

Answer 11

A-I ==ACE (in lungs)===> A-II A-II functions are as follows - Vasoconstriction => Raised BP - Vasoconstriction of Efferent arteriole of glomeruli => Increased Filtration fraction (FF) to preserve GFR - (+) Thirst (via Hypothalamus) - (+) Aldosterone & ADH release - Increases PCT Na+/H+ activity

Answer 12

Stimulated by - Raised A-II, K+ & ACTH levels - Causes retention of Na+ in exchange for K+/H+ in DCT

Answer 13

2 diseases causes 90% of HyperCa2+ Primary HyperPTH (MCC in Non-Hospitalized pts.) Malignancy (MCC in Hospitalized pts.) - PTHrP from tumour (Sq.CC of lungs) - Bone metastates - Myeloma (Osteoclastic bone resorption by local cytokines-IL1, TNF released by myeloma cells)

Answer 14

Sarcoidosis Vit. D intoxication Acromegaly Thyrotoxicosis Milk-Alkali syndrome Drugs: Thiazides, Ca2+ containing antacids Dehydration. Addison's. Paget's TB & Histioplasmosis (Hyper Ca2+ due to prolonged Immobilization)

Answer 15

Rehydration with NS (3- 4 lt./ day) Bisphosphonates (Takes 2 days to work with max. effect by 7 days) Other options are Clacitonin (quicker effect than Bisphosphonates) Sarcoidosis: STREOIDS Furosemide: In pts. who can't tolerate aggressive fluid rehydration (beware of Electrolyte imbalance)

Answer 16

AKI Drugs: K+ sparing diuretics, ACEi, ARBs, Ciclosporin Metabolic Acidosis Addison's Rhabdomyolysis Massive BT Beta blockers (interfere with K+ transport into cells) in Renal Failure UnFH & LMWH [by aldosterone secretion (-)]

Answer 17

IV Calcium Gluconate (To stabilize the Cardiac membrane) Short term K+ shift from ECF => ICF - Insulin + Dextrose infusion - Neb. Salbutamol Removal of K+ from body - Calcium Resonium (Enemas>Oral) - Loop Diuretics - Dialysis (If AKI + Persistent HyperK+)

Answer 18

Salt substitutes (contains K+ instead of Na+) Banana. Avocado Oranges. Spinach Kiwi fruit. Tomatoes

Answer 19

Haemolysis during Venipuncture - Excessive Vacuum while drawing - Prolonged tourniquet - Fine needle gauge Delay in processing of Blood specimen Myeloproliferative disorders (Abnormally high Plt., WBCs, RBCs) Familial causes

Answer 20

As K+ levels rise, fewer H+ ions can enter cells

Answer 21

A D condition - causes HTN + Hypo[K+] Alkalosis - Disordered Na+ channels in DCT => Increased Reabsorption of Na+ Rx.- - Amiloride or Triamterene

Answer 22

A R condition [SLC12A1 mutation] - Defect: Na+/K+/2Cl- (similar to using a Loop diuretics) - Normotension - HypoK+ - HYPERCALCIURIA - Polyuria, Polydipsia - Presents in CHILDHOOD: eg FTT

Answer 23

Defect in Thiazide sensitive Na+/Cl- transporter in the DCT [SLC12A3 mutation] - Normotension - Hypo K+ - HYPOCALCIURIA - Hypo Mg2+ - Met. ALKALOSIS

Answer 24

DCT defect (Inability to generate acid urine- secrete H+) - Causes: Idiopathic, RA, SLE, Sjogren's, Amphotericin B toxicity, Analgesic Nephropathy Complications - Nephrocalcinosis - Renal Stones

Answer 25

PCT defect (Decreased HCO3- Reabsorption) - Causes: Idiopathic, Fanconi's, Wilson's, CYSTINOSIS, Outdates Tetracyclines, CA inhibitors (Acetazolamide, Topiramate) Complications: Osteomalacia

Answer 26

Reduced Aldosterone ==> Reduced PCT [NH4-] excretion - Causes: Hypoaldosteronism, Diabetes Leads to HYPERKALAEMIA

Answer 27

Due to Carbonic Anhydrase 2 deficiency - Results in Hypokalaemia Extremely Rare

Answer 28

Hyperlipidaemia (increase in serum volume) Blood from drip arm

Answer 29

By Urinary Na+ & Osmolarity levels 1) Urinary Na+ > 20 mmol/l Na+ depletion (Renal loss): pts. are often hypovolaemic - Diuretics: Thiazides, Loop - Addison's - Diuretic stage of RF Pat. often Euvolaemic - SIADH (U Osml. > 500 mmol/kg) - Hypothyroidism 2) Urinary Na+ < 20 mmol/l

Answer 30

Na+ depletion, Extra renal loss - Diarrhoea, Vomiting, Sweating - Burns, Adenoma of Rectum Water Excess (Hypervolaemic & Oedematous) - 2ndary Hyperaldosteronism: HF, Liver cirrhosis - Nephrotic syndrome - IV Dextrose - Psychogenic Polydipsia

Answer 31

Develops over a period < 48hrs Develops over a period > 48 hrs - Mild: 130- 134 mmol/l - Moderate: 120- 129 mmol/l - Severe: < 120 mmol/l HYPOVOLAEMIC HypoNa+ or Clinically Dehydrated - Diuretic stage of RF, Diuretics - Addisonian Crisis EUVOLAEMIC HypoNa+ - SIADH HYPERVOLAEMIC HypoNa+ - HF, Liver failure, Nephrotic

Answer 32

Mild HypoNa+ may be Asymptomatic Early C/F - Headache, Lethargy, N & V, Dizziness, Confusion, Muscle cramps Late C/F - Seizures, Coma, Resp. Arrest

Answer 33

HYPOVOLAEMIC Suspected - Isotonic Saline 0.9% NaCl Can be given as trial => If Na+ level rises => supports Dx. - If Na+ levels falls => alternate Dx like SIADH EUVOLAEMIC Suspected - Fluid Restriction: 500-1000ml/day - Consider medications: Democlocycline & Vaptans HYPERVOLAEMIC Suspected - Fluid Restriction: 500-1000ml/day - Loop Diuretics & Vaptans

Answer 34

< 120 mmol/L - Hypertonic Saline (3% NaCl) is used to correct the Na+ levels more quickly than would be done in Chr. Hypo Na+

Answer 35

Dehydration Osmotic Diuresis eg.- Hyperosmolar Non-Ketotic Diabetic Coma Diabetic Insipidus Excessive IV Saline Should be corrected with CAUTION - Brain can lose Na+ & K+ rapidly, but lowering of other Osmolytes (specially H2O) occurs at a slower rate, predisposing to C- OEDEMA => Seizures, Coma & Death - Correction rate: <= 0.5 mmol/hr

Answer 36

Alcohol excess, Acute Liver Failure DKA, Refeeding syndrome Osteomalacia Primary HyperPTH CONSEQUENCES - RBC Haemolysis - WBCs & Platelets dysfunction - Muscle Weakness, Rhabdomyolysis - CNS Dysfunction

Answer 37

Liver: Cholestasis, Hepatitis, Fatty Liver, Neoplasia Paget's Osteomalacia HyperPTH Bone Metastases. Renal Failure Physiological: Pregnancy, Growing children, Healing #

Answer 38

- Bone Metastases & HyperPTH - Osteomalacia & Renal Failure

Answer 39

IL-1, IL-6, IL-8 & TNF-alpha stimulates liver to produce these proteins CRP Procalcitonin Ferritin. Haptoglobin Fibrinogen Alpha-1 Antitrypsin Caeruloplasmin Serum Amyloid A Serum Amyloid P component Complement

Answer 40

Synthesised by LIVER which binds to Phosphocholine in Bacterial cells & on cells undergoing Apoptosis - By binding =activate=> Complement - Also rise after a Surgery: > 150 at 48 hrs post-op. suggests evolving complications

Answer 41

Negative Acute phase proteins - Albumin - Transthyretin (formerly aka Prealbumin) - Transferrin - Retinol binding protein - Cortisol binding protein

Answer 42

Increased synthesis (rise in cell turnover) - Lesch-Nyhan - Myeloproliferative disorders - Diet rich in Purines. - Exercise - Psoriasis. - Cytotoxics Decreased Excretion - Drugs: Low-dose Aspirin, Pyrazinamide - Pre-Eclampsia - Alcohol. - Lead - Renal Failure

Answer 43

Chronic syndrome of impaired carbohydrate, protein & fat metabolism due to insufficient secretion of Insulin &/or Target-tissue Insulin resistance

Answer 44

Autoimmune disease => Antibodies against Beta cells of Pancreas - HLA DR4>HLA DR3 Various antibodies such as - Islet-Associated ANTIGEN 2 (IAA 2) - Glutamic Acid Decarboxylase GAD Antibody - Anti-ZnTransporter 8 Antibody

Answer 45

Polyuria, Polydipsia, Wt. loss May present with DKA - Abd. Pain - Vomiting - Reduced Consciousness level Picked incidentally on Routine Ix. Polydipsia, Polyuria Polyuria & Polydipsia are due to H2O being dragged out of the body due to osmotic effects of excess blood glucose => Glycosuria

Answer 46

Finger prick Bedside Glucose monitor One off BG (Fasting or Post-P) HbA1c OGTT Dx. is made by either Plasma glucose or HbA1c sample

Answer 47

1) If pt. is SYMPTOMATIC - FBG >= 7 mmol/L - Random BG or After 75g OGTT >= 11.1 mmol/L. (OR) 2) If pt. is ASYMPTOMATIC - Above criteria must be proved on 2 separate occasions. (OR) 3) HbA1c >= 48 mmol/L or 6.5% (but a value < 48 mmol/L does NOT exclude DM: cause it is not as sensitive as FBG)

Answer 48

FBG of >= 6.1 but < 7.0 mmol/L - Due to HEPATIC Insulin Resistance FBG of < 7.0 mmol/L & OGTT 2 hr value >= 7.8 but < 11.1 mmol/L - Due to MUSCLE Insulin Resistance IGT pts. are more likely to develop T2DM & CVS disease than IFG pts. People with IFG should be offered an OGTT to rule out dx. of DM

Answer 49

FBG of 6.1 to 6.9 mmol/L (OR) HbA1c b/w 42 to 47 mmol/L (6.0% to 6.4%) Normal HbA1c is <= 41 mmol/L (5.9%)

Answer 50

ToC: BASAL-BOLUS Regimen - Multiple daily injections of long acting Basal Insulin (eg.- Insulin Detemer or Glargine) + Rapid acting Insulin (eg.- Aspart) before meal 2x- daily PREMIXED INSULIN - Indicated if BB regimen is CI CSII (Continuous Subcutaneous Insulin Infusion) METFORMIN can be considered in pts. with BMI >= 25 kg/m2

Answer 51

Pts. with persistently HIGH HbA1c despite optimal injection regimens

Answer 52

5- 7 mmol/L upon WAKING 4- 7 mmol/L PRE-MEAL throughout the day Post-Meal targets is individualised based on risk of Hypoglycaemia HbA1c - Aim for <= 48 mmol/L (6.5%) unless limited by Hypoglycaemia or other factors - Measure every 3- 6 months

Answer 53

Assess CVS risk factor (High risk QRISK >= 10% or Established CVD or Chr. HF) - If Yes: METFORMIN & once established & titrated up as required, then add SGLT-2 i - If No: only METFORMIN IF Metformin is CI - CVD (+)ve: SGLT-2 monotherapy - No CVD: DPP-4 i/ Pioglitazone/ SUs & SGLT-2 can be used if NICE criterias are met

Answer 54

SECOND Line Add any 1 of the following to Metformin - DPP-4 i or Pioglitazone or SUs or SGLT-2 (if NICE criterias met) THIRD LINE Add another drug from the list above - eg.- Metformin + DPP-4 i + SUs (OR) Start Insulin-based Rx

Answer 55

Switch one of the drugs for GLP-1 mimetic IF - BMI >= 35 kg/m2 & specific psychological or other medical probs a/w Obesity (OR) - BMI < 35 & for whom Insulin Rx. will have occupational hazards or Wt. loss would benefit other Obesity-related comorbidities Should only be continued IF - HbA1c reduction of at least 11 mmol/L (1%) & Wt. loss of at least 3% of initial body wt. in 6 months GLP-1 mimetic should only be added to Insulin under specialist care

Answer 56

Metformin should be continued - Other OHAs, review the need Start with **Human NPH Insulin** - *Isophane (Intermediate-acting*) taken at Bed-time or 2x daily according to need

Answer 57

BBR (NPH or Long-acting analogs) when - HbA1c exceeds 58 mmol/L (7.5%) despite maximal OHAs - Continue Metformin & stop other OHAs if Complex Insulin regimen is initiated

Answer 58

At HbA1c of >= 58 mmol/L (7.5%) - If the BG is within this threshold (eg- 55 mmol/L, do not add another OHA) For Lifestyle/ Metformin: Target is <= 48 mmol/L Add-on therapy: <= 53 mmol/L Frail/ Elderly: Relaxed, Case-dependent [HbA1c should be checked every 3- 6 months until stable, then 6 monthly]

Answer 59

BLOOD PRESSURE - In < 80yrs old: < 135/85 mmHg - In > 80yrs old: < 145/85 mmHg - ACEi or ARBs are 1st line in HTN LIPID Management - High intensity Statin (eg Atorva 20-80 mg) for primary or 2ndary prevention - LDL Cholesterol targets: High Risk pts.: < 1.8 mmol/L & Very High Risk pts.: < 1.4 mmol/L ANTI-PLATELETS - For 2ndary prevention in pts. with established CVD

Answer 60

Regular RFT monitoring - eGFR & ACR Use SGLT-2 i for renal protection in Albuminuric CKD Optimize BP control with ACEi/ ARBs

Answer 61

Adjust Medication Timing & Dosing - Split Metformin doses: 1/3rd pre-sunrise (Suhoor) & 2/3rd post-sunset (Iftar) - Shift SUs to evening dose with Iftar - No adjustments needed for Pioglitazone Pts. with chronic conditions are exempt from fasting or may be able to delay fasting to shorter days of winter months Foods recommended - Suhoor: Long acting Carbohydrates - BG moniter is given so that they can check their glucose levels

Answer 62

RAPID Acting (Onset: 15 min) - Peak: 1-2 hrs, Duration: 3-5 hrs - Insulin Lispro, Aspart, Glulisine SHORT Acting (Onset: 30 min) - Peak: 2-4 hrs. Duration: 5- 8 hrs - Regular Insulin (Humulin R, Novolin R) INTERMEDIATE Acting (Onset: 1-2 hrs) - Peak: 4- 12 hrs, Duration: 4-12 hrs - NPH Insulin LONG Acting Insulin (Onset: 1- 2 hrs) - Duration: 20- 24 hrs - Insulin Glargine, Detemir

Answer 63

Preferred initial regimen in T1DM - BBR Insulin adjustments required in Infections & Stress conditions S/E - Lipodystrophy at injection site - Hypoglycaemia, Wt. gain

Answer 64

- (-)Hepatic Gluconeogenesis, - Improves peripheral insulin sensitivity; - Reduces Intestinal Glucose absorption CI: eGFR < 30 ml/min; Acute or Chronic Met. Acidosis S/E: GI upset- N and Diarrhoea;Lactic acidosis; Avoid in Acutely ill pt.

Answer 65

(+) Pancreatic Beta-cell Insulin release by blocking ATP-sensitive K+ channel Gliclazide, Glimepiride, Glibenclamide - Short acting (Gliclazide) preferred S/E: Hypoglycaemia (MC with Long acting one); Wt. gain; Rare: Hypo Na+ & Bone marrow Suppression CI: Pregnancy & Breastfeeding

Answer 66

PPAR-Gamma agonists - Increases Insulin Sensitivity in Fat, Muscles & Liver - Promotes Adipogenesis & Fatty Acid storage S/E: Wt. gain; Fluid retention; Risk of #, Increased risk of Bladder Ca CI: HF (NYHA 3 or 4) Monitor LFT & Minimal Hypoglycaemia

Answer 67

Risk of Lower Limb Amputation

Answer 68

(-) DPP-4 enzyme => Prolongs action of INCRETINS (GLP-1, GIP) => Enhance Glucose-dependant Insulin release - Suppress Glucagon Sitagliptan, Vildagliptan, Saxagliptan S/E: Pancreatitis CI: Pts. with Pancreatitis Wt. Neutral Useful in Older/ Frail pts. where Hypoglycaemia is a concern

Answer 69

(-) SGLT-2 in Renal Tubules - Reduces Glucose reabsorption - Increases Urinary Glucose excretion Empa-, Dapa-, Cana- Gliflozin Indication: T2DM, High CVD or Renal risk, HFrEF S/E: UTI & Genital TI ; EUGLYCAEMIC Ketoacidosis CI: eGFR < 45 ml/min Cardio- & Nephro- Protective

Answer 70

Mimics GLP-1 to (+) Insulin secretion, (-) Glucagon, Slow gastric emptying & Promote Satiety S/E: N & V (MC), Diarrhoea, Pancreatitis (Rare), Medullary Thyroid CA (caution in FHx of MEN-2)

Answer 71

Dual GLP-1 & GIP receptor Agonist - (+) Insulin secretion, (-) Glucagon & Improves metabolic outcomes S/E: N & V; Hypoglycaemia (rare, when combined with Insulin or SUs) Promotes Significant Wt. loss Cardioprotective benefits seen

Answer 72

Injectables: Liraglutide, Exenatide, Dulaglutide Oral: Semaglutide (taken in empty tummy, 30 min before food) GLP-1r Agonists can be continued if - > 11 mmol/L (1%) fall in HbA1c levels in 6 months - 3% wt. loss in 6 months Exenetide is a/w Severe Pancreatitis

Answer 73

C/F - Erratic BG control, Bloating & Vomiting Chr. Diarrhoea: MC at Night Rx.- - Metoclopramide, Domperidone or Erythromycin

Answer 74

PAGeD Amitriptyline, Duloxetine, Gabapentin or Pregabalin - Do NOT use these in combination Rescue Therapy: TRAMADOL Topical Capsaicin for localised neuropathic pain (Post-Herpatic N)

Answer 75

Lipids - Start in pts. with QRISK > 10% (10 year CV risk) PRIMARY Prevention (QRISK > 10% or T1 DM or CKD if eGFR < 60 ml/min): - Atorva 20 mg SECONDARY Prevention (IHD or Cerebrovascular disease or PAD) - Atorva 80 mg ANTI-PLATELETS - Offered only if pt. has existing Cardiovascular disease

Answer 76

2nd MC medical disorder complicating pregnancy (after HTN) Risk Factors - BMI > 30 kg/m2 - PHx of Macrosomic baby >4.5 kg - PHx of GDM - 1st degree relative with DM - Family origin with a high prevalence of DM (South Asian, Black Carribbean, Middle East)

Answer 77

Test of Choice: OGTT (Early self-monitoring of BG is an alternative) - Women with PHx of GDM: OGTT asap after Booking & at 24-28 POG - Women with RFs: OGTT at 24-28 wks Diagnostic Criteria - FBG: >= 5.6 mmol/L - 2 hr Glucose: >= 7.8 mmol/L

Answer 78

1) If FBG < 7 mmol/L: Trial of Diet & Exercise should be offered - If target BG is not met in 1- 2 wks => Start METFORMIN - If BG targets still not met: add Insulin- Short-acting only (to the existing regimen) 2) If FBG >= 7 mmol/L at Dx.: INSULIN is started directly 3) If FBG b/w 6.0 to 6.9 + Evedence of complications (Macrosomia/ Hydramnios) : INSULIN is started 4) If Metformin not tolerated + decline Insulin Rx : GLIBENCLAMIDE can be offered

Answer 79

Wt. loss if BMI > 27 kg/m2 Stop OHAs except Metformin Start INSULIN - Folate 5 mg/ day from Preconception to 12 wks POG - Detailed ANOMALY Scan at 20 wks including 4 chamber view of heart & Outflow tracts - Tight Glycaemic control Treat RETINOPATHY as it can worsen during pregnancy

Answer 80

FBG: 5.3 mmol/L 1 hr PP: 7.8 mmol/L 2 hrs PP: 6.4 mmol/L

Answer 81

T2 DM in < 25 yrs old A D condition MODY 3: 60% cases - Defect in HNF-1 alpha gene - a/w increased risk of HCC MODY 2: 20% cases - Defect in GF (Glucokinase) gene MODY 5: (Rare) - Defect in HNF-1 Beta gene - a/w Liver & Renal cysts

Answer 82

Ketosis is NOT a feature at presentation Very Sensitive to SULFONYLYREAS - Insulin is not usually necessary

Answer 83

Glycaemic Index - White Rice (87), Baked potato (85), White Bread (70) - Couscous (65), Boiled New Potato (62), Digestive Biscuits (59), Brown Rice (58) - Fruits & Vegetables, Peanuts

Answer 84

HbA1c is produced by glycosylation of Hb at a rate proportional to the Glucose conc. Lower-than-expected levels of HbA1c (due to reduced RBCs life span) - SCD - G6PD deficiency - Hereditary Spherocytosis HIGHER-than-expected levels of HbA1c (due to increased RBCs life span) - B12 or Folate Deficiency, IDA - Splenectomy

Answer 85

Ave. P. Glucose = (2*HbA1c) - 4.5

Answer 86

- Insulinoma (increased Proinsulin : Insulin ratio) - Self administration of Insulin or SUs - Liver Failure - Addison's Alcohol (Exaggerated Insulin secretion) - [-OH] => affects Pancreatic Micro-circulation => Blood redistribution from exocrine to Endocrine part => Increased Insulin secretion - Nesidioblastoma (Beta cell Hyperplasia)

Answer 87

BG < 3.3 mmol/L cause AUTONOMIC C/F due to Glucagon & Adrenaline release - Sweating, Shaking, Hunger, Anxiety, Nausea BG < 2.8 mmol/L cause NEURO-GLYCOPENIC C/F due to inadequate Glucose supply to the brain - Weakness, Vision changes, Confusion, Dizziness Severe & Uncommon C/F - Convulsions & Coma

Answer 88

Occurs 2ndary to 2 main factors - NEUROPATHY: Loss of protective sensation, Charcot's arthropathy, Dry skin - PAD: Macro & Micro vascular complication Features - Neuropathy: Loss of sensation - Ischaemia: absent foot pulses, reduced ABPI, intermittent claudication - Complications: Calluses, ulcerations, Charcot's arthropathy, cellulitis, Osteomyelitis, Gangrene

Answer 89

Screened on an ANNUAL Baasis - Screening for ischaemia: Palpate both Dorsalis oedis & Poste. Tibial pulses - Screening for Neuropathy: 10g Monofilament is used on various parts of the foot Moderate/ High risk pts. should be followed up regularly by the Local Diabetic Foot Centre

Answer 90

LOW Risk: Only Callus MODERATE Risk: Deformity/ Neuropathy/ Non-Critical limb ischaemia HIGH Risk: - Previous ulceration or - Previous amputation - On Renal R T or - [Neuropathy + Non-Critical L I] or - Neuropathy + Callus &/or Deformity - Non-Critical L I + Callus &/or Deformity

Answer 91

Complication of T1DM or 1st presentation of T1DM - Uncontrolled LIPOLYSIS => excess FAs released => Ketone bodies RFs: Infection, Missed Insulin, MI C/F - Abd. Pain, - Polyuria, - Polydipsia - Dehydration - Kussmaul breathing (Deep HyperV) - Acetone breath ('Pear drops' smell)

Answer 92

BG > 11 mmol/L or known DM pH < 7.3 HCO3- < 15 mmol/L Ketones > 3 mmol/L (OR) Urine Ketones ++ on dipstick

Answer 93

Fluid Replacement - DKA pts. are deplete around 5-8 lt. - Isotonic NS used initially INSULIN - IV infusion at 0.1 U/kg/hr - Once BG < 15 mmol/l, 5% Dextrose infusion is started Correction of Electrolyte Imbalance - S K+ is high despite low total body K+ - Falls quickly once Insulin Rx. started - K+ is added to fluids - If rate of K+ infusion is > 20 mmol/hr , Cardiac monitoring is required LONG Acting Insulin continued & Short acting Insulin is stopped

Answer 94

0.9% NS 1L over 1st hour 0.9% NS 1L + KCl over next 2 hrs 0.9% NS 1L + KCL over next 2 hrs 0.9% NS 1L + KCl over next 4 hrs 0.9% NS 1L + KCl over next 4 hrs 0.9% NS 1L + KCl over next 6 hrs SLOWER Infusion rate indicated in YOUNG pts. (18- 25) as they are higher risk of Cerebral Oedema

Answer 95

K+ levels in 1st 24 hrs is - > 5.5 mmol/L : Nil replacement - 3.5- 5.5 : 40 mmol/L - < 3.5 : Senior review as additional K+ needs to be given

Answer 96

pH > 7.3 Blood Ketones < 0.6 mmol/L HCO3- > 15.0 mmol/L Ketonemia & Acidosis should be resolved in <= 24hrs if NOT => Senior review from Endocrinologist Above criteria met + pt. is eating & drinking, Switch to SC Insulin Diabetes Specialist Nurse review before discharge

Answer 97

Gastric Stasis Thromboembolism Arrhythmias 2ndary to Hyper[K+] or Iatrogenic Hypo[K+] - Iatrogenic: Incorrect Fluid therapy => Cerebral Oedema, Hypo[K+], Hypoglycaemia ARDS & AKI

Answer 98

Highly vulnerable to Cerebral Oedema following Fluid Resuscitation - Often needs 1:1 nursing to monitor CNS signs- Headache, Irritability, FND, Visual probs - Usually occurs 4- 12 hrs following commencement of Rx. but can present at any time - Any suspicion: CT head + Senior review

Answer 99

Medical emergency, Elderly with T2DM, extremely difficult to manage - Hyperglycaemia => Osmotic Diuresis , Severe Dehydration & Electrolyte imbalance - Severe Volume depletion => significantly raised Serum Osml. typically > 320 mosml/kg => Blood Hyperviscosity

Answer 100

Hypertonicity leads to preservation of Intravascular volume

Answer 101

- Fatigue, Lethargy, N & V - CNS: Altered Sensorium, Headaches, Papilloedema, Weakness - HYPERVISCOSITY: MI, Stroke, Peripheral Arterial Thrombosis - CVS: Hypotension, Tachycardia, Dehydration

Answer 102

- Hypovolaemia - Marked Hyperglycaemia > 30 mmol/L without significant Ketonaemia or Acidosis - Significantly raised S Osmolarity > 320 mosml/kg Mixed DKA & HHS can occur

Answer 103

1) Normalise OSMOLALITY (Gradual) - Key parameter to monitor 2) Replace Fluid & Electrolyte losses - Fluid replacement alone will cause a gradual decline in BG & Osml. - Insulin Rx. prior to adequate fluid replacement => CV collapse as H2O moves out of Intravascular space => decline in Intravascular volume Ketone is measured before the need of Insulin is assessed - IF Ketonaemia (+): Beta-hydroxy butyrate > 1 mmol/L; indicates relative HypoInsulinaemia & Insulin is started (eg.- Mixed DKA/HHS) - Fixed rate IV Insulin infusion given at 0.05 U/kg/hr

Answer 104

Fluid loss in HHS is around 100- 220 ml/g ; 10- 22 lt. in 100kg man Rate of Rehydration is assed by - Initial severity - Pre-existing co-morbidities (HF, CKD, Elderly) 1st line fluid: IV 0.9% NS - This is Hypotonic => very effective in restoring Normal S Osml. - Achieve a (+)ve balance of 3-6 lt. by 12 hrs & remaining replacement fluid in next 12 hrs - Rx. Aim: Replace 50% estimated fluid loss in 1st 12 hrs & rest in the following 12 hrs (if co-morbidities present limit correction speed) - If S Osml. not declining despite (+)ve balance with 0.9%NS switch to 0.45% NS

Answer 105

2*[Na+] + Glucose + Urea

Answer 106

Reduction of S. Osml. will cause a shift of H2O into Intracellular space - This Inevitably results in rise in Na+ - Normally, Fall in BG of 5.5 mmol/L results in a 2.4 mmol/L rise in Na+ - IF this rise is > 2.4 for each 5.5 fall in BG, this suggests INADEQUATE Fluid replacementy - Rise in Na+ is a concern if Osml. is NOT declining concurrently - Safe rate of fall of BG: 4- 6 mmol/hr - Fall of Na+ should not exceed 10 mmol/L in 24 hrs Target BG: b/w 10- 15 mmol/L Complete normalization of Electrolyte & Osml. takes up to 72 hrs

Answer 107

High Insulin, Raised Proinsulin : Insulin ratio - High C-Peptide Supervised, prolonged fasting (72hrs) CT Pancreas Treatment - Surgery - Diazoxide & Somatostatin if Sx CI

Answer 108

Fredrickson type 3 Hyperlipidaemia or Broad-Beta disease or Dysbetalipoproteinaemia - Mixed Hyperlipidaemia (Raised Ch. & TGs levels) - a/w APO-E2 Homozygosity - High incidence of IHD & PVD Impaired removal of INTERMEDIATE Density Lipoprotein from the blood by the Liver

Answer 109

In the COMMUNITY - Oral Glucose 10- 20 g in liquid, gel or tablet form - Alternate: GlucoGel or DextroGel - A HypoKit can be prescribed (Glucagon vial for IM/ SC at home) In HOSPITAL Setting - Alert: Quick acting Carbohydrate (as above) - Unconscious/ Unable to swallow: IM or SC Glucagon injection - Alternate: IV 20% Glucose solution

Answer 110

Neuroendocrine Tumour & MC Pancreatic Endocrine tumour Site: Islet of Langerhans cells - 10% malignant, 10% multiple - 50% have MEN-1 Early morning hypoglycaemia or just before meals eg.- Diplopia, Weakness - Raised body wt.

Answer 111

It is a cluster of abnormalities - INSULIN RESISTANCE - IGT - Central Obesity - Reduced HDL Ch. levels - Elevated TGs - HTN Key pathogenesis factor: Insulin Resistance Other associated features include - Raised Uric Acid levels - NAFLD, PCOS

Answer 112

SIMON-BROOME Criteria In Adults: TC > 7.5 & LDL-C > 4.9 In Children: TC >6.7 & LDL-C > 4.0 For definitive FH - Tendon Xanthoma in pts. (OR) - 1st or 2nd degree relatives (OR) - DNA evidence of FH For Possible FH - FHx of MI in < 50yrs in 2nd degree relative (OR) - < 60 yrs in 1st degree relative (OR) - FHx of raised Ch. levels

Answer 113

Referral to specialist Lipid Clinic - 1st line: High dose Statins - 1st degree relative have a 50% chance of having the disorder, so should be offered screening - Statins should be discontinued in women 3 months before conception

Answer 114

Selectively & Competitively (-) HMG-CoA Reductase => decreases Ch. biosynthesis in Liver => Increases no. of Hepatic LDL receptors on Cell surface => Enhanced uptake & Catabolism of LDL S/E: Myalgia, less frequently- Myositis or Rhabdomyolysis

Answer 115

A D condition; results in High levels of LDL Ch. - Due to mutations in the gene which encodes LDL-receptor protein When to Suspect this ?? - Total Ch. > 7.5 mmol/L &/or - Personal or FHx of Premature CAD (event when < 60yrs in an index person or 1st degree relative) Children of affected parents - If 1 parent : Test Child by age 10yrs -If Both parents: Test by 5 yrs of age

Answer 116

- Yellow Palmar Crease - Palmar Xanthomas - Tuberous Xanthomas Treatment - 1st line: FIBRATES

Answer 117

HYPER- TGs predominant - DM type 1 & 2, - Obesity - Alcohol. - Liver disease - Chr. Renal Failure - Drugs: Thiazides, Non-selective Beta blockers, Unopposed Oestrogen HYPER- Ch. predominant - Nephrotic syndrome - Cholestasis - Hypothyroidism

Answer 118

LIPOPHILLIC Statins - Atorva-, Lova-, Simva-, Fluva-, Pitava- HYDROPHILLIC Statin - Pravastatin - Rosuvastatin Lipophillic statins are widely distributed in various tissue but Hydrophillic statins are Liver specific - S/E of statins are MC with Lipophillic

Answer 119

Specially used in Hyper TGs - Activates PPAR-Alpha receptors => Increase in LPL activity => Reduce TGs - Peroxisome proliferator-activated r S/E: - GIT s/e are common - Increased risk of Thromboembolism

Answer 120

(-) intestinal absorption of Ch. by blocking Neimann-Pick C1-Like 1 (NPC1L1) protein transporter on Intestinal & Hepatic cells - Decreases delivery of intestinal Ch. to liver Indications - Primary Heterozygous-Familial & Non-Familial Hyper Ch.

Answer 121

Monotherapy - Primary Hyper Ch. in adults in whom Statins are CI or can't tolerate it Co-Admistered with Initial Statin Rx. - Primary Hyper Ch. in adults who have started Statin therapy when --- TC or LDL-C not well controlled either after proper dose titration of initial Rx. or because dose titration is limited by intolerance to initial statin therapy --- Change from initial Statin therapy to an alternative statin is being considered

Answer 122

Adenosine Triphosphate Citrate Lyase (ACL) Inhibitor Indications - Primary Hyper Ch (Heterozygous Familial & Non- Familial) - Mixed dyslipidaemia - Pts. unable to reach LDL-C goal with max. tolerated dose of statin - Statins are not tolerated or CI

Answer 123

Proprotein Convertase Subtilisin/ Kexin Type 9 There are 2 FDA approved drugs - Alirocumab (Praluent) SC - Evolocumab (repatha) SC - Both are available as Pre-filled pen Indications - Hyper Ch & Mixed Dyslipidaemia - Homozygous Familial Hyper Ch - Established Atherosclerotic CVS disease

Answer 124

PCSK9 (-) stop the protein from working => more LDL r are available on liver cells => lower Blood Ch - Normally PCSK9 protein breaks down LDL receptors => less receptor available & Blood Ch rises Prescription - Used in combination with Statin or Statin with other lipid-lowering therapies in pats. unable to reach - LDL-C goals with max. tolerated dose of Statin or Alone or in combination with other lipid-lowering Rx. in pts. who are Statin intolerant or Statin is CI

Answer 125

Hashimoto's thyroiditis (MCC) - Autoimmune, a/w T1DM, Addison's, Pernicious anaemia - Can cause transient thyrotoxicosis in acute phase - 5x- 10x MC in Women Subacute thyroiditis (De Quervain's) - a/w painful goitre & raised ESR Reidel's thyroiditis - Painless goitre - Fibrous tissue replace normal tissue Postpartum Thyroiditis Drugs: Lithium, Amiodarone Iodine deficiency - MCC in developing world

Answer 126

1) Grave's disease (MCC) - Typical thyrotixicosis features + Thyroid eye disease 2) Toxic Multinodular Goitre - Autonomously functioning thyroid nodule => secretes excess thyroxine 3) Drugs: AMIODARONE 4) ACUTE Phase of - Subacute (De Quervain's) thyroiditis - Post-Partum Thyroiditis - Hashimoto's

Answer 127

Wt. gain, Lethargy, Cold Intolerance Skin: Dry, Cold, Yellowish skin - Non-Pitting oedema (hands & face) - Dry, Coarse scalp hairs, loss of lateral eyebrows Constipation Menorrhagia CHS: Decreased DTRs, Carpel Tunnel Syndrome

Answer 128

Wt. loss, Manic, Restlessness, Heat Intolerance CVS: Palpitations, Arrhythmias (AF) Skin: Increased sweating - Periorbital Myxoedema: Erythematous, oedematous lesions above lateral malleoli - Thyroid Acropachy: Clubbing Diarrhoea Oligomenorrhoea CNS: Anxiety, Tremors

Answer 129

Anti-TPO antibody TSH receptor Antibody TG Antibodies There is significant overlap but - TSH r Antibody: Grave's - Anti-TPO Antibody: Hashimoto's

Answer 130

1) EYE Signs (30% cases) - Exophthalmos - Ophthalmoplegia 2) Pretibial Myxoedema 3) Thyroid Acropachy (TRIAD) - Digital Clubbing - Soft tissue swelling of hands & feet - Periosteal New bone formation

Answer 131

TSH r stimulating Antibody (90%) Anti-TPO antibodies (75%) Thyroid Scintigraphy - Diffuse, Homogenous, increased uptake of Radioactive Iodine

Answer 132

Initial Rx (control of c/f) - PROPRANOLOL (blocks adrenergic effects) Refer to 2ndary Care for ongoing Rx Carbimazole is considered in Primary care if pts. c/f are NOT controlled with Propranolol 1st line: Anti-Thyroid drugs ATD Titration Regimen - CARBIMAZOLE started at 40mg, reduced gradually to maintain Euthyroidism; - Taken for 12-18 months 'Block & Replace' is Alternate Rx. - Carbimazole 40mg & Thyroxine is added when pt. becomes Euthyroid - Taken for 6- 9 months ATD has fewer S/E than B & R RADIOIODINE Rx.

Answer 133

Used in pts. who relapse to ATD therapy or are Resistant to primary ATD Rx. Absolute CI - Pregnancy (avoid for 4- 6 months after Rx) - < 16 yrs old Relative CI: Thyroid Eye disease Maj. of pts. will require Thyroxine Rx. by 5 yrs after RI Rx.

Answer 134

Plummer's Disease Autonomously functioning Thyroid nodules => Hyperthyroidism - Nuclear Scintigraphy: PATCHY Uptake ToC: RADIOIODINE Therapy

Answer 135

Autoimmune response against an Autoantigen, possibly TSH r => Retro-Orbital Inflammation => GAGs & Collagen deposition in the Muscles SMOKING (most imp. RFs for devt. of Thyroid eye disease) RadioIodine Rx. can aggravate inflam. of Thyroid eye disease

Answer 136

Exophthalmos, Conjunctival Oedema Optic Disc Swelling Ophthalmoplegia Inability to close eyelids => Sore, dry eyes ==> Exposure Keratopathy Treatment - Topical Lubricants - Steroids - Radiotherapy - Surgery

Answer 137

- Unexplained deterioration in Vision - Awareness of change in intensity or quality of colour vision in 1 or both eyes - H/o Eye suddenly 'popping out' (Globe subluxation) - Obvious Corneal Opacity - Cornea still visible when eyelids are closed - Disc swelling

Answer 138

Iatrogenic Thyroxine excess do NOT usually result in thyroid storm RFs - Thyroid or Non-Thyroidal Sx - Trauma, Infection - Acute Iodine load (CT contrast) C/F - Fever > 38.5 C - Tachycardia, HTN, HF - N & V; Confusion & Agitation - Abnormal LFTs- Jaundice clinically Treatment - PCM, Treat the Ppt. event - IV Propranolol - Methimazole or PTU - Lugol's Iodine - Dexamethasone: 4mg IV qds =(-)=> T4 to T3 conversion

Answer 139

Chronic Autoimmune Thyroiditis - a/w Hypothyroid - Transient Thyrotoxicosis seen in acute phase - 10x MC in women A/W: Coeliac's, T1DM, Vitiligo O/E: Firm, Non-tender Anti-TPO (+)ve also Anti-TG antibodies

Answer 140

MALT Lymphoma

Answer 141

De Quervain's Thyroiditis - Subacute GRANULOMATOUS Thyroiditis - Occurs after a VIRAL Infection - Presents with Hyperthyroidism Thyroid Scintigraphy - Globally REDUCED I-131 uptake Rx.: Self-limiting - Thyroid pain: Aspirin, NSAIDs - STEROIDS in more severe cases particularly if Hyperthyroidism (+)

Answer 142

Phase-1 (3- 6 wks): - Hyperthyroid, Painful goitre - Raised ESR Phase-2 (1- 3 wks): Euthyroid Phase-3 (wks- months): Hypothyroid Phase-4 : Thyroid str. & function goes back to normal

Answer 143

Normal Free T4 & T3 levels + TSH < 0.1 mu/l Causes - MNG (particularly in Elderly females) - EXCESS Thyroxine may give a similar biochemical result Treatment - TSH levels must be persistently low to warrant intervention - Therapeutic level Low-dose ATD for 6 months (to induce remission)

Answer 144

Causes - MNG in elderly females - EXCESS Thyroxine Effects - CVS- Atrial Fib. - Osteoporosis - Increased risk of Dementia

Answer 145

Raised TSH & T3, T4 normal No obvious C/F Treatment 1) TSH b/w 4- 10mU/L + Free T4 within normal range - If < 65yrs + C/F of HypoT: LevoT trial => if NO improvement => Stop LevoT - Older pts. (> 80yrs old): Watch & Wait, usually avoid hormonal Rx - Asymptomatic: Observe & Repeat TFT in 6 months 2) TSH > 10 mU/L + Free T4 in normal range - < 70yrs: LevoT started even if Asymptomatic - Older people (> 80yrs old): Watch & Wait, hormone Rx. is generally avoided

Answer 146

Sick Euthyroid Syndrome - TSH, T3, T4 all are LOW - In maj. TSH is in Normal range (inappropriate as T3 & T4 are low) Reversible upon recovery from systemic illness => NO Rx.

Answer 147

Dense Fibrous tissue replacing the Normal thyroid parenchyma - O/E: Hard, Fixed, Painless goitre - Middle aged female - a/w Retroperitoneal Fibrosis

Answer 148

Affects 1 in 4000 babies - If NOT dx. & treated within 1st 4 wks => Irreversible Cognitive Impairment C/F - Prolonged Neonatal Jaundice - Delayed mental & physical milestones - Short stature - Puffy face, Macroglossia - Hypotonia Babies screened at 5- 7 days with Heel Prick test

Answer 149

A R condition; characterised by - B/L SNHL - Mild Hypothyroidism - Goitre Defect in ORGANIFICATION of I- => Dyshormonogenesis - Thyroid C/F are mild & pts. are often Euthyroid - Progressive Hearing loss, delay in academic progression

Answer 150

TFTs are Normal PERCHLORATE Discharge test aids Dx Gene testing: PDS gene on Chr 7 Audiometry & MRI: Characteristic 1.5 turns in the Cochlea (normal 2.5) Treatment - Thyroid Hormone Replacement - Cochlear Implant

Answer 151

Head trauma can worsen SNHL [IM pts. should also avoid for 4 to 6 wks due to risk of Splenic rupture)

Answer 152

Blocks TPO from Coupling & Iodinating the Tyrosine residues on TGs => reduce T hormone synthesis PTU as well as this central MoA, it also has a Peripheral action - (-) 5-deiodinase which reduces peripheral T4 to T3 conversion S/E: Agranulocytosis - Crosses Placenta (but can be used in low doses during pregnancy)

Answer 153

In pregnancy, there is an increase in TBG levels; this causes an - INCREASE in Total Thyroxine levels - Do NOT affect Free Thyroxine Beta-HCG can activate TSH r => Transient Gestational HyperT MCC of Thyrotoxicosis in Pregnancy is Grave's disease

Answer 154

1st Trimester: PTU - Carbimazole is a/w increased risk of congenital abnormalities At the beginning of 2nd Trimester - switch back to CARBIMAZOLE Maternal F T4 levels are kept at upper 1/3rd of normal range to avoid Fetal Hypothyroidism RadioIodine therapy is CI

Answer 155

Thyroxine is SAFE - TSH is measured in each Trimester & 6- 8 wks post-partum INCREASE dose of Thyroxine- - By 50% as early as 4- 6 wks POG Breastfeeding is SAFE while on Thyroxine

Answer 156

To determine the risk of Neonatal Thyroid Problems

Answer 157

PAPILLART (70%) - Often young female, good prognosis FOLLICULAR (20%) MEDULLARY (5%) - Cancer of Parafollicular (C) cells, secrete Calcitonin, part of MEN-2 ANAPLASTIC (1%) - Not responsive to Rx., Pressure c/f LYMPHOMA (rare) - a/w Hashimoto's

Answer 158

- Contains a mixture of Papillary & Colloidal filled follicles - HP: Papillary projections & pale empty nuclei - Seldom encapsulated - LN metastasis predominant - Blood spread is rare

Answer 159

Present as SOLITARY Thyroid Nodule Malignancy can only be excluded on formal HP assessment

Answer 160

Macroscopically encapsulated, Microscopically Capsular Invasion is seen- without this finding, the lesion is a Follicular Adenoma Vascular Invasion predominates Multifocal disease is rare

Answer 161

C-cells derived from Neural Crest & NOT thyroid tissue S. Calcitonin levels are often raised Familial form in 20% cases LN & Blood metastasis recognised Nodal disease is a/w poor prognosis

Answer 162

Elderly Females (MC) Local Invasion is a common feature Rx.- Resection if possible - Palliation may be achieved through Isthmusectomy & Radiotherapy - Chemo is NOT effective

Answer 163

Dry (Anhydrosis), Cold, Yellow skin Non-pitting oedema (eg- Hand, face) Dry, coarse scalp hair, loss of lateral part of eyebrow Eczema Xanthomata Pruritus

Answer 164

Pretibial Myxoedema - Erythematous, Oedematous lesions above the lateral malleoli - Thyroid acropachy - Scalp hair thinning - Increased sweating - Pruritus

Answer 165

Elderly female + Thirst + inappropriately normal or Raised PTH Causes - SOLITARY ADENOMA (MCC) 80% - Hyperplasia (15%) - Multiple adenoma (4%) - Carcinoma (1%) a/w HTN & MEN-1 & MEN-2

Answer 166

Bones, stones, abd. groans & psychic moans - Polydipsia, Polyuria - Depression - Anorexia, Nausea, Constipation - PUD - Pancreatitis - Bone pain/ # - Renal stones - HTN

Answer 167

- Raised Ca2+ & Low PO4- - PTH may be raised or Normal (inappropriate as Ca2+ is raised) - Tc.-MIBI Subtraction scan - X-Ray Skull: Pepperpot Skull Definitive Rx.- Total PTectomy Conservative Rx. - If Ca2+ < 0.25 mmol/L above upper limit & Pt. is > 50yrs & No evidence of End organ damage Sx. CI: Cinacalcet (a Calcimimetic) - Mimics the action of Ca2+ on tissue by allosteric activation of Ca2+ sensing receptors

Answer 168

- Generalised Osteopenia - Acro-Osteolysis: Erosions of Terminal Phalangeal tufts - Sub-periosteal resorption of bone

Answer 169

A D condition Target cell insensitivity to PTH due to mutation in a G-protein - Type-1: Complete receptor defect - Type-2: Cell receptor intact Bloods: - High PTH, Low Ca2+, High PO4-

Answer 170

Short 4th & 5th Metacarpals Short stature Cognitive impairment Obesity Round face

Answer 171

PTH infusion => measure Urinary PO4- & cAMP - Type-1: Neither of them rises - Type-2: cAMP rises but Urine PO4- do not change

Answer 172

Seen after PTectomy if HyperPTH has been long standing High Pre-op PTH levels => constant (+) of Osteoclast activity=> Bone Demineralized => HyperCa2+ On PTectomy => PTH levels drop rapidly (due to short 1/2 life) => Osteoclast activity diminishes => Bone rapidly begins to Remineralize => Hungry Bone syndrome

Answer 173

X-ray: Changes similar to Metastatic Lytic lesions if left untreated Effects on Ca2+ levels - Hypocalcaemia

Answer 174

Benign tumour of Pituitary G - Most cases are asymptomatic & is an Incidental Dx. Classification based on SIZE: Microadenoma (< 1cm) & Macroadenoma (> 1cm) Hormone Status: - Secretory/ Functioning adenoma: Produces a hormone in excess - Non-Secretory adenoma: do NOT produce hormone in excess

Answer 175

1) PROLACTINOMAS (MC type) 2) Non-Secreting Adenomas: next MC type 3) GH Secreting 4) ACTH Secreting

Answer 176

1) Excess of a Hormone - Prolactin excess: Amenorrhoea & Galactorrhoea - ACTH excess: Cushing disease - GH excess: Acromegaly 2) DEPLETION of a Hormone (due to Compression of normal functioning Pituitary gland) - Non-Functioning tumours: Generalised Hypopituitarism 3) Stretching of the Dura (in/around pituitary fossa): Headaches 4) Compression of Optic Chiasma - Bitemporal Hemianopia (nasal fibre

Answer 177

Pituitary Blood Profile - GH, Prolactin, ACTH, FH, LH, TFTs Formal Visual Field Testing MRI Brain with Contrast Rx.- - Hormonal Therapy: Bromocriptine 1st line for PLomas - Surgery: Transsphenoidal Transnasal Hypophysectomy - Radiotherapy

Answer 178

Causes: - 95% cases are 2ndary to Pituitary Adenoma - Ectopic GNRH or GH production by tumour eg.- Pancreas Complications - HTN, - DM - Cardiomyopathy - COLO-RECTAL Cancer

Answer 179

- Coarse facial appearance, Spade like hands, Increase in Shoe size - Large tongue, Prognathism, Interdental spaces - Excess Sweat & Oily skin: Sweat gland hypertrophy - Pituitary Tumour C/F: Hypopituitarism ,Headache, Bitemporal Hemianopia - Raised PL 1/3rd case: Galactorrhoea - MEN-1 in 6% cases

Answer 180

1st line: Serum IGF-1 levels - If elevated confirm with Serial GH measurements (lack of suppression of GH < 1 ug/L following documented Hyperglycaemia during an OGTT [Normally GH is suppressed to < 2 mu/L with Hyperglycaemia] Monitoring: Serum IGF-1 MRI of Pituitary to show tumour

Answer 181

1st line: Trans-sphenoidal Sx If Inoperable or Sx. unsuccessful SOMATOSTATIN Analogue - Directly (-) release of GH - eg.- Octreotide - Effective in 50- 70% cases PEGVISOMANT - GH receptor antagonist: (-) GH receptor dimerization - SC administration once daily - Very effective - Do NOT shrink tumour; Sx needed DA Agonists - Bromocriptine - Now not used commonly EXTERNAL IRRADIATION - used in Older pts. or - Failed Sx. or Medical Rx.

Answer 182

Secreted by Anterior Pituitary gland - DA is the primary PL releasing Inhibitory factor - DA agonists (Bromocriptine) are used to control Galactorrhoea Features of PL Excess - Men: Impotence, Loss of Libido - Women: Amenorrhoea - Galactorrhoea in both M & F

Answer 183

Prolactinoma Pregnancy Oestrogens Physiological: Stress, Exercise, Sleep Acromegaly: 1/3rd pts. PCOS Primary Hypothyroidism: Because TRH (+) PL release

Answer 184

Metoclopramide, Domperidone Phenothiazines Haloperidol Very rare: SSRIs, Opioids

Answer 185

Malignancy - Small Cell Lung Ca - Also: Pancreas, Prostate CNS: Stroke, SAH, SDH, Meningitis/Abscess/Encephalitis Infections: TP, Pneumonia Drugs: - SUs (Glimepiride & Glipizide) - SSRIs, TCAs, Carbamazepine - Vincristine, Cyclophosphamide Other Causes - (+)ve End-Resp. Pressure [PEEP] - Porphyrias

Answer 186

Excess ADH hoemone produced => excess H2O retention => HypoNa+ 2ndary to dilutional effect Rx.- - Slow correction of HypoNa+ - Fluid restriction - Democlocycline: reduces response of Collecting Duct to ADH - ADH r Antagonists

Answer 187

Used in the Ix. of HYPOPITUITARISM - IV Insulin is given => GH & Cortisol levels measured - Normal Pituitary: Both rises Contraindications: - Epilepsy - IHD - Adrenal Insufficiency

Answer 188

It is designed to help evaluate pts. who have POLYDIPSIA - Normal: Urine Osm- > 600 & Urine osm. Post DDAVP- > 600 - Psychogenic Polydipsia: U Osm- > 400 & U osm Post DDAVP: > 400 - Cranial DI: U Osm- < 300 & U Osm Post DDAVP- > 600 - Nephrogenic DI: U Osm < 300 & U Osm Post DDAVP- < 300

Answer 189

MCC: B/L Idiopathic Adrenal Hyperplasia (70%) Conn's syndrome Features HTN + Hypo[K+] - Muscle weakness Alkalosis

Answer 190

1st line: Plasma Aldosterone : Renin ratio - High Aldosterone & Low Renin [(-)ve feedback from Na+ retention] Differentiate b/w U/L or B/L cause - HRCT Abdomen & Venous Sampling If CT is normal - Adrenal Venous Sampling can be used to differentiate b/w U/L Adenoma & B/L Hyperplasia

Answer 191

Adrenal Adenoma: SURGERY B/L Adereno-Cortical Hyperplasia - Aldosterone antagonists (Spironolactone)

Answer 192

Inadequate synthesis of Adrenal hormones- Cortisol & in some cases, Aldosterone due to dysfunction at Adrenals/ Pituitary/ Hypothalamus Types PRIMARY Adrenal I (PAI) - Adrenal failure - Addison's is the MC form of PAI - Other Causes: Infections, Adrenal haemorrhage, Metastatic Ca, CAH SECONDARY Adrenal I (SAI) - Decreased ACTH from Pituitary - Chr. GC Therapy, Pituitary Tumour or Pituitary Sx. TERTIARY Adrenal I (TAI) - Decreased CRH from Hypothalamus - Due to Prolonged suppression by Exogenous GCs

Answer 193

PAI - Adrenal Cortex damage => Low Cortisol & Aldosterone, High ACTH - Hyperpigmentation, Hypotension, Hypo[Na+] & Hyper[K+] SAI & TAI - Deficient ACTH (SAI) & CRH (TAI) production - Aldosterone secretion is PRESERVED as it is primarily regulated by RAAS - NO electrolyte abnormalities but Cortisol deficiency C/F like Fatigue, Weakness, Adrenal crisis under stress

Answer 194

PAI is more severe at presentation C/F common to all forms of AI - Fatigue, Lethargy - Muscle weakness - Wt. loss - N & V - Hypotension (Orthostatic) C/F specific to PAI - Hyperpigmentation [elevated ACTH also (+) MSH receptors] - Hypo[Na+] & Hyper[K+] - Salt craving (hallmark of Aldosterone deficiency) SAI & TAI - NO hyperpigmentation & electrolyte abnormality

Answer 195

INITIAL Tests 1) 8 am Serum Cortisol test - 150 nmol/L: Highly suggestive of AI - 150- 300 nmol/L: Uncertain; further testing with ACTH Stimulation - > 300 nmol/L: AI unlikely 2) SYNACTHEN Test (ACTH (+) test) - Used to CONFIRM the dx. of AI & differentiate b/w PAI & SAI/TAI - In PAI: Cortisol levels fail to rise after ACTH administration - In SAI/TAI: Blunted response seen, but some Cortisol increase may occur 3) ACTH Levels: - PAI: Elevated ACTH (due to lack of Cortisol (-)ve feedback - SAI/TAI: Low or Normal ACTH

Answer 196

S. Electrolytes - In PAI only: Hypo[Na+] & Hyper[K+] due to aldosterone deficiency Renin & Aldosterone levels: Useful in confirming Aldosterone deficiency in PAI

Answer 197

GC Replacement - 1st line: Hydrocortisone in divided dose - 15- 25 mg/day (2 or 3 divided dose)\ - Largest dose: Morning & Smaller dose later in the day (to avoid INSOMNIA) MC Replacement - Necessary in PAI (eg. Addison's) - Fludrocortisone 50- 300 mcg/day

Answer 198

2x or 3x the GCs dose during - Illness, Sx., or Maj. stress to avoid Adrenal Crisis - IM Hydrocortisone if pt. unable to take Oral medications (eg. N & V)

Answer 199

Regular Monitoring of - BP, Electrolytes, Signs of GCs under- or over- replacement Bone Density - Assessed periodically due to risk of GC induced Osteoporosis

Answer 200

MCC of Primary Hypoadrenalism in the UK accounting for 80% cases - Both Cortisol & Aldosterone are reduced Lethargy, Weakness, Anorexia, N & V, Wt. loss, SALT Craving Hyperpigmentation (specially Palmar Crease) Vitiligo, loss of Pubic hairs in women, Hypotension, Hypoglycaemia Hypo[Na+] & Hyper[K+] may be seen

Answer 201

PRIMARY Cause - TB, -HIV, -APLS - Metastases (eg. Bronchial CA) - Waterhouse-Friderichsen syndrome (Meningococcal Septicaemia) SECONDARY Causes - Pituitary Causes (eg- Tumors, Irradiation, Infiltration) EXOGENOUS GC Therapy

Answer 202

Definitive Ix.- Synacthen Test (ACTH Stimulation Test) If Synacthen test NOT available=> 9 am S. Cortisol - > 500 nmol/L: Addison's unlikely - < 100 nmol/L: Definitely abnormal - 100- 500 nmol/L: Do Synacthen test Electrolyte Abnormalities

Answer 203

Hyper[K+] Hypo[Na+] Hypoglycaemia Met. Acidosis

Answer 204

Causes - Sepsis or Surgery causes acute exacerbation of Chr. Insufficiency (Addison's, Hypopituitarism) - Adrenal Bleeding eg- Waterhouse F synd. (Fulminant Meningococcemia) - Steroid withdrawal

Answer 205

- Hydrocortisone 100mg IM or IV - 1 lt. NS infusion over 30-60 min or with Dextrose if Hypoglycaemic - Continue Hydrocort 6 hrly until pt. is stable - NO Fludrocortisone (High Cortisol exerts Weak MC action) - Oral Replacement: After 24 hrs & be reduced to maintenance dose over 3- 4 days.

Answer 206

ACTH Dependent Causes - Cushing's disease (80%): Pituitary tumour secreting ACTH => Adrenal Hyperplasia - Ectopic ACTH production (5- 10%): Small Cell Lung Ca. is the MCC ACTH Independent Causes - Iatrogenic: Steroids - Adrenal adenoma (5- 10%) - Adrenal CA (rare) - CARNEY Complex ( syndrome including Cardiac Myxoma) - Micronodular Adrenal Dysplasia (very rare) PSEUDO-Cushing's

Answer 207

- Mimics Cushing's - Often due to [-OH] excess or Severe Depression - Cause FALSE (+)ve Dexamethasone Supression test or 24hr Urinary Free Cortisol - Insulin Stress test may be used to differentiate

Answer 208

Iatrogenic: Corticosteroids therapy ACTH Dependent Causes - Cushing's Disease: P adenoma => ACTH secretion) - Ectopic ACTH secretion 2ndary to Malignancy ACTH Independent Causes - Adrenal Adenoma

Answer 209

1) 1st line: Overnight Dexamethasone Suppression Test - Most sensitive test - Cushing's pts. do NOT have morning Cortisol spike suppressed 2) 24 hrs Urinary Free Cortisol

Answer 210

1st line: 9 am & Midnight plasma ACTH (& Cortisol) levels - ACTH suppressed: Non-ACTH dependent cause is likely (A Adenoma High-Dose DM Suppresion Test - Used to localise the pathology resulting in Cushing's Synd.

Answer 211

Cushing's Syndrome due to other causes (eg.- Adrenal Adenomas) - Cortisol: NOT suppressed - ACTH: Suppressed Cushing's Disease (ie. P Adenoma => ACTH secretion) - Cortisol: Suppressed - ACTH: Suppressed Ectopic ACTH syndrome - Cortisol: Not suppressed - ACTH: Not suppressed

Answer 212

If Pituitary source: Cortisol rises If Ectopic/ Adrenal: NO change in Cortisol Petrosal Sinus sampling of ACTH - To differentiate b/w Pituitary & Ectopic ACTH secretion

Answer 213

Insulin Stress Test

Answer 214

Petrosal Sinus sampling of ACTH

Answer 215

Used in cases of Primary Pituitary Dysfunction - Given: Insulin, TRH, LHRH - Measured: S. Glucose, Cortisol, GH, TSH, LH, FSH levels are recorded at regular intervals PL levels are sometimes measured - DA antagonist test: Normal response is 2x rise in PL. A Blunted response suggests- Prolactinoma - Metoclopramide is used in Ix. of HyperPL

Answer 216

- GH levels rises > 20 mu/l - Cortisol level rises > 550 mmol/l - TSH level rises by > 2 mu/l from baseline - LH & FSH should double

Answer 217

Catecholamine secreting tumour - 10% are Familial & may be a/w MEN-2, NF & VHL syndrome - B/L in 10% - Malignant in 10% - Extra-adrenal in 10%

Answer 218

Typically Episodic - HTN (90%, may be sustained) - Headache, - Palpitations - Anxiety, - Sweating IxoC: 24hr Urinary Metanephrine levels (97% Sensitive) - 24hr Urinary Catecholamines (86% sensitive) Rx.- - ToC: SURGERY Pt. should be 1st stabilised with drugs - Alpha blockers (eg. Phenoxybenzamine) given BEFORE a - Beta blocker (Propranolol)

Answer 219

Cluster of at least >= 2 endocrine diseases in a pt. attributed to Autoimmunity - LYMPHOCYTE Infiltration causes organ specific damage TYPES (PAS-2 is Commonest) - PAS-1: Multiple Endocrine Deficiency Autoimmune Candidiasis (MEDAC) - PAS-2: Schmidt's Syndrome (MC) - X-linked Immune Dysregulation Poly Endocrinopathy & Enteropathy (IPEX) - Iatrogenic Poly-endocrinopathy due to use of Immunoregulatory agents in pts. with cancer

Answer 220

Onset: Children; M:F=3:4; Triad of - Adrenal Insufficiency - Chr. Hypoparathyroidism - Chr. CANDIDIASIS A R condition; Monogenic; AIRE1 gene mutation on Chr 21 A/W the following - T1DM, - Pernicious anaemia - Thyroid disorder, - IgA deficiency - Alopecia, - Vitiligo - Chr. Active Hepatitis - Chr. Atopic Dermatitis - KCS, - Hypogonadism

Answer 221

Onset: Childhood to adult; M:F=1:3 MC than PAS-1; At least 2/3 of - Autoimmune Adrenal I - Autoimmune Thyroid disease (Graves or Hypothyroidism) - T1DM Complex Polygenic Inheritance Links to HLA DR3 & DR4 A/W the following - Premature Ovarian deficiency - Vitiligo, - Coeliac's - Hypoparathyroidism - Chr. Atrophic Gastritis & B12 deficiency

Answer 222

46 XY [X linked recessive disorder] - Defective Androgen receptor => End-organ resistance to Testosterone => Female Phenotypes & Male Genotype - Rudimentary Vagina & Testes but No uterus - Testosterone, Oestrogen & LH are all elevated

Answer 223

- Primary Amenorrhoea - Undescended testes => Groin swelling - Breast develops: Conversion of Testosterone => Oestradiol Dx.- Buccal Smear or Chr. Analysis Rx.- - Raise child as Female - B/L Orchidectomy - Oestrogen therapy

Answer 224

46 XY [A R condition] - Inability of Males to convert Testosterone to DHT - Ambiguous genitalia at Newborn - Hypospadiasis is common - Virilization at puberty

Answer 225

46 XY - Has Testes but external genitilia are female's or ambiguous - May be 2ndary to AIS

Answer 226

46 XX - Has Ovaries but external genitalia are Male's (virilized) or ambiguous - May be 2ndary to CAH

Answer 227

46 XX or 47 XXY - Both Ovarian & Testicular tissue are present

Answer 228

Primary Hypogonadism (Klinefelter's) - LH: High & Testosterone: Low Hypogonadotrophic hypogonadism (Kallman's syndrome) - LH: Low & T: Low AIS - LH: High & T: Normal/High Testosterone secreting syndrome - LH: Low & T: High

Answer 229

47 XXY - Taller than average - Lacks 2ndary Sexual character - Small, Firm testes; - Infertile - Gynaecomastia: increased breast Ca risk - Elevated Gonadotrophin levels Dx.: Chromosomal Analysis

Answer 230

Recognised due to delayed puberty 2ndary to hypogonadotrophic hypogonadism - X-linked Recessive trait Failure of GnRH-secreting neurons to migrate to hypothalamus Defect in Olfactory neurons- - Hyposmia or Anosmia

Answer 231

- Delayed Puberty, - ANOSMIA - Hypogonadism, Cryptorchidism - Sex hormone levels are LOW - LH, FSH are inappropriately low /normal - Pts. are typically of normal or above average height Dx.- Cleft lip/Palate & Visual/Hearing defects are seen in some pts.

Answer 232

A R disorders - Affects ADRENAL Steroid Biosynthesis Due to Low Cortisol levels => Anterior Pituitary secretes High levels of ACTH =(+)=> Adrenal Androgens synthesis => virilize Female infants

Answer 233

21-Hydroxylase Deficiency (90%) - Female: Genitalia virilised - Males: Precocious puberty - 60- 70% pts. have a Salt-losing crisis at 1- 3 wks. of age 11-Beta Hydroxylase Deficiency (5%) - Female: Genitalia Virilised - Males: Precocious Puberty - HTN + Hypo[K+] 17-Hydroxylase Deficiency (Rare) - Females: Non-Virilising - Boys: Inter-sex - HTN

Answer 234

Abnormal amount of Breast tissue in Males - Due to Increased Oestrogen : Androgen ratio - Differentiate Gynaecomastia from Galactorrhoea (due to action of PL on Breast tissue) GRADES- - 1: Small enlargement, No excess Skin - 2a : Moderate enlargement + No excess Skin - 2b : Moderate enlargement + Extra skin - 3 : Marked enlargement + Extra Skin

Answer 235

Puberty (Normal) Kallman's, Klinefelter's Testicular Failure eg- Mumps Liver disease Testicular Ca eg.- Seminoma secreting hCG Ectopic tumour secretion Hyperthyroidism Haemolysis Drugs

Answer 236

MCC: Spironolactone Cimetidine Digoxin Cannabis Finasteride GnRH agonists (Goserelin, Buserelin) Oestrogen, Anabilic steroids Very Rare Causes - TCAs, - Isoniazid, - CCBs - Heroin, - Busulfan, - Methyldopa

Answer 237

Menses : 1- 4th day Follicular [Proliferative] : 5- 13th day Ovulation : 14th day Luteal [Secretory] : 15- 28th day

Answer 238

- No. follicle develops => only One follicle will become Dominant around Mid-Follicular phase - Proliferation of Endometrium FSH rises (devt. of follicles) => secretes Oestradiol; When Egg has matured => secretes enough Oestradiol to =(+)=> LH surge => Ovulation Cervical Mucus- - After Menses: Thick & Pluged Ext. Os - Prior to Ovulation : Clear, Acellular, Low Viscosity - 'Stretchy'- "Spinnbarkeit" BB Temp.- Falls prior to Ovulation (Oestradiol influence)

Answer 239

Corpus Luteum Endometrium: Changes to Secretory lining under Progesterone influence C Luteum => secretes Progesterone rises through Luteal phase => If no fertilization => CL degenerates => P falls & Oestradiol levels rise in Luteal Cervical Mucus - Thick, Scanty & Tacky (due to P) BB Temp.- Rises post ovulation in response to higher P levels

Answer 240

No Menses by 15 yrs + normal 2ndary Sex. characters (OR) by 13 yrs without 2ndary sex. characteristics CAUSES - MCC: Gonadal dysgenesis (Turner's) - Testicular Feminization - Congenital Genital tract malformed - Functional Hypothalamic Amenorrhoea (eg.- 2ndary to Anorexia) - CAH - Imperforate Hymen

Answer 241

Menses stop for 3- 6 months in Women with previous normal & regular menses (OR) 6- 12 months in women with H/o Oligomenorrhoea CAUSES (exclude Pregnancy) -Hypothalamic Amenorrhoea (2ndary to Stress, Excess Exercise) - Hyperprolactinaemia - Premature Ovarian Failure - Thyrotoxicosis, - PCOS - Sheehan's, - Asherman's (IU adhesions) HYPOTHYROIDISM can also cause Amenorrhoea

Answer 242

EXCLUDE Pregnancy Gonadotrophins - Low levels : Hypothalamic cause - High levels : Ovarian problem - Raised if Gonadal Dysgenesis (eg.- Turner's) Prolactin Androgen levels - Raised levels can be seen in PCOS Oestradiol FBC, U&E, Coeliac's screen, TFTs

Answer 243

PRIMARY Amenorrhoea - Ix. & Rx of root cause - Primary Ovarian Insufficiency due to Gonadal dysgenesis (Turner's): HRT SECONDARY Amenorrhoea - EXCLUDE Pregnancy, Lactation & Menopause (in >= 40 yrs old) - Treat the underlying cause

Answer 244

Ovarian Dysfunction - Hyperinsulinaemia & High levels of LH is common in PCOS - Overlaps with Metabolic Syndrome Subfertility or Infertility Oligo- or Amenorrhoea Hirsutism, Acne (Hyperandrogenism) Obesity Acanthosis nigricans (Insulin R)

Answer 245

Pelvic USS: Multiple cysts in Ovaries PL is normal or elevated Testosterone is normal or elevated SHBG is low or normal Raised LH:FSH (classic feature is no longer useful Check of Impaired Glucose Tolerance

Answer 246

Rotterdam Criteria [2/3 must be (+)] - Infrequent/ No Ovulation (presents as infrequent/no menses) - Hyperandrogenism (Hirsutism, Acne (OR) elevated Total/Free Testosterone levels) - Polycystic Ovaries on USS (>= 12 follicles of 2-9 mm) in one or both ovaries (OR) Increased Ovarian Volume > 10 cm3

Answer 247

Wt. Loss COCPs (If Contraception needed) Hirsutism & Acne - 1st line: COCPs - 2nd line: Topical Eflornithine - Spironolactone, Flutamide, Finasteride used under specialists INFERTILITY - Wt. Loss - Clomephene (risk of Multiple pregnancies) - Metformin: alone or combined with Clomephene specially in Obese pts. - Gonadotrophins

Answer 248

3rd Generation COCPs (OR) - Due to Fewer S/E Co-Cyprindol - Anti-androgen Both has risk of VTE

Answer 249

Menopausal C/F + Elevated Gonadotrophins in < 40 yrs old C/F - Climacteric c/f: Hot flushes, Night sweats - Infertility - 2ndary Amenorrhoea Raised FSH & LH - FSH > 40 IU/l - Elevated FSH should be shown in 2 blood sample 4- 6 wks apart Low Oestradiol - eg.- < 100 pmol/l

Answer 250

IDIOPATHIC (MCC) - FHx may be (+)ve B/L Oophorectomy Radio & Chemo therapy Infection (eg.- Mumps) Autoimmune disorders Resistant Ovary Synd.- FSH receptor abnormalities Rx.- - HRT or COCPs until 51 yrs (average age of menopause)

Answer 251

5th MC malignancy in Females - Peak: 60 yrs & carries poor prognosis due to late Dx. Epithelial origin (90%): with 70-80% cases due to Serous CA Site of Origin: Distal F tubes RFs - FHx of BRCA1 or BRCA2 mutation - Multiple Ovulations: Early menarche, Late Menopause, Nulliparous Multiple pregnancies & COCPs are protective

Answer 252

Notoriously Vague C/F - Abd. distension & Bloating - Abd. & Pelvic Pain - Urinary C.F eg- Urhency - Early Satiety, - Diarrhoea Ix. Initial Test: CA-125 - If >= 35 IU/L => Urgent USS of Abd. & Pelvis CA-125 should NOT be used for screening

Answer 253

Diagnostic Laparotomy Rx.- Surgery + Chemo (Platinum based) Prognosis: 80% have advanced disease at presentation

Answer 254

Ovarian cancer Endometriosis Menstruation Benign Ovarian Cysts

Answer 255

Smooth muscle tumours of Uterus - Seen in 20% White & 50% Black women in later Reproductive years. - MC in Afro-Caribbean Women - Rare before puberty, develops in response to Oestrogen Dx.- TV-USS

Answer 256

- May be Asymptomatic - Menorrhagia: Can cause IDA - Lower Abd. Pain: Cramping, common during Menses - Bloating - Urinary C/F: Frequency (with large fibroids) - Subfertility - POLYCYTHAEMIA 2ndary to EPO production by the fibroid

Answer 257

Asymptomatic: NO Rx. + periodic review to monitor size & growth Rx. of Menorrhagia LNG-IUS : Useful if Contraception is also required - Can't be used if Uterine cavity distorted NSAIDs, Tranexemic Acid, COCPs Oral or Injectable Progestogen Rx. to Shrink/ Remove Fibroids Medical: - GnRH agonists: Shrinks but useful for short term Rx - Ulipristal Acetate: used in the past Surgical: Uterine Artery Embolization

Answer 258

Myomectomy: can be performed Abdominally, Laparoscopically or Hysteroscopically Hysteroscopic Endometrial Ablation Hysterectomy Regress after Menopause Complications - Sub-fertility & IDA - RED Degeneration- Haemorrhage into tumour: commonly occurs during Pregnancy

Answer 259

50% occurs in women < 45 yrs of age - Incidence rate highest in 25- 29 yrs Types - Squamous C Ca (80%) - Adenocarcinoma (20%) Features - Detected during Routine Cervical Screening - Abnormal Vag. Bleed: Postcoital, Intermenstrual or PM Bleed - Vaginal Discharge

Answer 260

HPV 16, 18 & 33 (most imp.) - 16 & 18 produces oncogene E6 & E7 - E6 (-) p53 Tumour Suppressor gene - E7 (-) RB suppressor gene Other RFs - Smoking, - HIV - Early 1st Coitus, - High Parity - Many Sexual Partners - Low SES - COCPs

Answer 261

MC in PM Women; but 25% cases are seen before Menopause Features - PM Bleed (classic symptom) - Intermenstrual Bleed in Pre-M women - Pain & Discharge (unusual)

Answer 262

Obesity, Nulliparity Early Menarche & Late Menopause Unopposed Oestrogen - Adding Progesterone reduces risk DM, PCOS, HNPCC Tamoxifen

Answer 263

PM bleed + >= 55 yrs - Refer via Suspected Ca Pathway 1st line: TV-USS - Normal endometrial thickness (< 4mm) has High (-)ve Predictive value Hysteroscopy with Biopsy Rx.- - Local disease: TAH + B/L S-O - High risk disease: TAH + B/L S-O + Post-Op. Radiotherapy - Progesterone Therapy (if Sx. is CI)

Answer 264

COCPs & Smoking

Answer 265

One of the top 5 causes of Ca in children, accounts for 7-8% of childhood malignancies - Site: Neural crest tissue of Adrenal Medulla (MC site) & SNS - Median age of onset: 20 months

Answer 266

Abdominal mass or Lump on Chest Pallor, Wt. loss Bone Pain, Limp Hepatomegaly Paraplegia Proptosis Ix.- Raised VMA & Homovanillic Acid (HVA) levels - Calcification on Abd. X-ray - Biopsy

Answer 267

A R condition; due to absence of - Galactose-1-Phosphate Uridyl Transferase - Results in Intracellular accumulation of Galactose-1-Phosphate Features- - Jaundice, - FTT, - Hepatomegaly - Cataracts, - Fanconi Syndrome - Hypoglycaemia after exposure to Galactose Dx.- Urine Reducing Substances Rx.- Galactose free diet If milk is given => Unmetabolised milk sugars build up & damage Liver, Eyes, Kidneys & Brain

Answer 268

Overactive Bladder/Urge Incontinence - Detrusor Overactivity - Urge to Urinate is quickly followed by uncontrollable leakage ranging from few drops to complete voiding STRESS Incontinence - Urine leak while Coughing/ Laughing MIXED Incontinence: - Both Urge & Stress OVERFLOW Incontinence - Bladder outlet obstruction eg Prostatomegaly FUNCTIONAL Incontinence

Answer 269

Bladder dairies for 3 days Vaginal examination to exclude Pelvic organ prolapse & ability to initiate voluntary contraction of pelvic floor muscles (Kegel exercise) Urine dipstick & Culture Urodynamics studies

Answer 270

Comorbid physical conditions impair the pts. ability to go to a bathroom in time Causes: Dementia, Sedating drugs & Injuries/ Illness => decreased Ambulation

Answer 271

Bladder Retraining ( for >= 6 wks; gradually increase interval b/w voiding) Bladder Stabilising Drugs - 1st line: Anti-Muscuranics - Immediate release: Oxybutynin, Tolterodine - Once daily: Darifenacin - Immediate release is avoided in Frail elderly pts. MIRABEGRON (Beta-3-agonist) - Used if anti-cholinergic S/E is a concern in elderly, frail pts.

Answer 272

Pelvic Floor Muscle Training - 8 contractions; 3x/day for 3 months Sx.- Retropubic Mid-Urethral Tape procedure Sx. declined: Duloxetine - Combined NE & Serotonin reuptake inhibitor - Increase synaptic conc. of NE & Serotonin in Pudendal nerve => increased (+) of urethral striated muscles within the sphincter enhanced

Answer 273

Nephrotic Synd. Cholestasis Hypothyroidism DM, Alcohol Bendrofluazide (Increases both Ch. & TGs) Obesity- - Elevated TGs - Low HDL-C - Slightly elevated LDL-C

Answer 274

Generally Dx. due to their compressive C/Fb(eg. Visual probs.) - May manifest with Pan-Hypopituitarism due to compression of normally functioning pituitary ToC: Trans-sphenoidal Sx.

Answer 275

Non-Functioning Pituitary adenoma

Answer 276

Medullary (in MEN 2) Papillary

Answer 277

Lithium, Democlocycline, OFLOXACIN, Orlistat PTH levels

Answer 278

Test sensation using 10g Monofilament

Answer 279

TSH normal/low; T4: low; T3: low Non-thyroidal Illness syndrome aka Euthyroid Sick Syndrome TSH: High; T3: High; T4: Normal

Endocrinology Flashcards

(323 cards)