Endocrine system Flashcards

Question

What are the Ix for diabetic ketoacidosis What parameters need to be monitored?

Answer 1

KING UFC - K+ (potassium supplementation) - Insulin - NG tube - Glucose (once serum levels drop) - Urea (monitoring kidneys) - Fluids - Creatinine (monitor)

Answer 2

Last line when uncertain (normally not necessary) USG: structural and obstructive lesions, hydronephrosis, asessment of renal size Renal biopsy: only if the the dx of diabetic nephropathy is uncertain

Answer 3

 Visual loss * Macular edema * Pre-retinal or vitreous hemorrhage (from neovascularization) * Traction retinal detachment * Neovascular glaucoma  Floaters * Retinal tear

Answer 4

1.  DM presenting with diabetic ketoacidosis (DKA)  Differential diagnosis for a high anion gap acidosis (↑ H+) * Lactic acidosis * Salicylate overdose * Methanol poisoning * Neurological causes o Stroke o Head injury 2.  Plasma glucose, ketones, electrolytes  Urine ketones  Blood-gas analysis  Look for precipitating infections * Respiratory * Gastrointestinal * Septicemia * Meningitis

Answer 5

 Fluid replacement therapy with large volume of isotonic saline * IV K+ replacement is likely to be required * Polyuria will persist until glucose level is normalized  IV Short-acting insulin  IV bicarbonate (HCO3-) * Only indicated in severe acidosis (pH > 7.0) since admission of alkali is associated with serious side effects such as hypokalemia and paradoxical acidosis of CSF  Remarks * Frequent monitoring of serum K+ and glucose level * Central line is useful to guide therapy especially in elderly with concomitant cardiac dysfunction * Underlying infection should be treated  Subcutaneous insulin injection * After the patient is stabilized  Diabetic education * Need of insulin treatment and insulin self-administration * Self-monitoring of BG * Recognition and treatment of hypoglycemia  Reinforcement of “sick-day rule” * More frequent monitoring of BG and check urine or blood for ketones during illness  Marked hyperglycemia requires temporary adjustment of insulin regimen  Seek medical advice if hyperglycemia is accompanied by ketosis

Answer 6

1.  Diabetic nephropathy leading to fluid overload * Diabetic nephropathy is clinically defined by persistent proteinuria > 500 mg/ 24 hours (24-hour urine collection) in patient with DM without other renal disease  Diabetic retinopathy * Dot and blot hemorrhages  Ischemic heart disease * Suggested by presence of chest pain * Macrovascular complication of diabetes 2.  Diabetic glomerulosclerosis * Consequence of ECM deposition in glomeruli  Nodular glomerulosclerosis * Along with typical Kimmelstiel-Wilson nodules  Mesangial cell expansion  Arteriolar hyalinosis * Leads to ischemic changes 3.  Assessment of renal function: CrCl (timed urine collection), eGFR using accepted equation  Urinalysis: Performed to look for infection or hematuria  Quantification of proteinuria  USG kidneys: Assess renal size or morphology, exclude obstruction and other concomitant lesions

Answer 7

 BP control by * ACEI/ ARI * β-blocker * CCB * Diuretics  Remarks * Evidence shows beneficial reno-protective effect of using ACEI or ARB * Hyperkalemia is a potential concern and should be monitored in these patients Drugs that are partially excreted via kidneys (can cause hypoglycemia especially in elderly with reduced renal function) e.g. chlorpropamide Biguanides: avoided since it can predispose to lactic acidosis in the presence of renal impairment

Answer 8

Solute or osmotic diuresis Glucose diuresis- Uncontrolled DM Urea diuresis oTissue catabolism o High-protein diet Sodium diuresis o Normal saline infusion o Bilateral urinary tract obstruction

Answer 9

 Polyuria * Defined as urine output > 3L/day in adults and > 2L/m2 in children  Polydipsia  Nocturia * Urine is most concentrated in the morning due to lack of fluid ingestion overnight and increased ADH secretion during late sleep period * First manifestation of a mild to moderate loss of concentrating ability is therefore nocturia

Answer 10

* GHS PTA = Good Hope School Parent-Teacher Association o GH = Growth hormone deficiency --> o S = Sex hormone (LH and FSH) deficiency --> o P = Prolactin --> o T = Thyroid hormone deficiency (Hypothyroidism) --> o A = ACTH deficiency

Answer 11

* Lactotroph adenoma* > * Non-functioning adenoma (25 – 35%) > * Somatotroph adenoma > * Corticotroph adenoma

Answer 12

* CBC with DC: baseline to prep patient for thionamides which can cause agranulocytosis * LFT: baseline LFT to prep patient for thionamides which can cause hepatotoxicity * TFT: do not use TSH level to monitor response to treatment since it can remain suppressed for several months (use T3 and T4 level instead) * TSH: most sensitive indicator of thyroid function due to short t1/2 * fT4 level, fT3 level * Thyroid antibdoies: anti TSH antibiodies, anti TPO antibdoies, anti TG (thyroglobulin) antibodies Radiological * Thyroid USG * FNA if compatible with sonographic criteria * Radionuclide scan (scintigraphy 99tc)

Answer 13

 Serum total T4 is a measurement of total T4 bounded to plasma binding proteins including thyroxine-binding globulin (TBG) and thyroxine-binding prealbumin (TBPA)  Plasma binding proteins are affected by diseased state * ↑ in pregnancy * ↓ in hypoalbuminemia

Answer 14

Serum IGF-1 + OGTT (confirm if GH is not suppressible) + pituitary MI

Answer 15

* Check ring size of the patient * X-ray heel for heel-pad thickness

Answer 16

 Signs that suggest adrenal tumour is the underlying cause * Palpable abdominal mass * Gynecomastia in males * Virilization in female  Signs that suggest ectopic ACTH production the underlying cause * Absence of Cushingoid body habitus * More prominent edema and hypertension * More prominent muscle weakness

Answer 17

 General conditions * Hypertension (60 - 80%) * Dyslipidemia (40 – 70%) * Overweight/ Obesity (90%) * Diabetes mellitus/ IGT (65%)  CNS system * Major depression and anxiety disorders (55 – 80%) * Impaired memory * Sleeping disturbance * Psychosis  MSS system * Osteoporosis * Proximal muscle weakness and wasting

Answer 18

GFR MGS (salt, sugar, sex) Zona glomerulosa (outer zone): mineralocorticoids (aldosterone) Zona fasciculata (midle zone): glucocorticoids (cortisol) Zona reticularis (inner zone): sex hormones (DHEAS) Adrenal medulla --> epinephrine and norepinephrine

Answer 19

 Screening test * Plasma aldosterone concentration (PAC) * Plasma renin activity (PRA) * Plasma aldosterone-to-renin ratio (ARR)  Confirmatory test (one of the four test) *** Oral sodium loading test * Saline infusion test** * Fludrocortisone suppression test * Captopril challenge test

Answer 20

 Autoimmune adrenalitis is the most common cause of primary adrenal insufficiency which is a process that worsens over a period of many months or years * Stage 1 = High plasma renin activity; Normal/ Low serum aldosterone * Stage 2 = Impaired serum cortisol response to ACTH stimulation * Stage 3 = Increasing morning plasma ACH with normal serum cortisol * Stage 4 = Low morning serum cortisol and overt clinical adrenal insufficiency

Answer 21

 CT adrenals * Small non-calcified adrenals in autoimmune causes * Enlarge calcified adrenal in tuberculosis, metastatic disease and hemorrhage  MRI pituitary * Evaluate for any anatomical abnormalities

Answer 22

 2 Most common causes * Hyperparathyroidism * Hypercalcemia of malignancy (secretion of PTH-like peptide)  Less common causes * Excess intake of vitamin D or calcium * Hyperthyroidism * Familial hypocalciuric hypercalcemia * TB * Sarcoidosis  Serum albumin, phosphate, PTH, alkaline phosphatase (ALP) * ↑ PTH, ↑ Ca2+, ↓ PO4- suggests hyperparathyroidism * ↓ PTH, ↑ Ca2+ suggests hypercalcemia of malignancy  24-hour urinary Ca2+ excretion  RFT

Answer 23

 Investigations are targeted at defining possible complications due to increase PTH levels and hypercalcemia  24-hour urinary Ca2+ excretion * Document degree of hypercalciuria  RFT  Abdominal X-ray and USG kidneys * Detect stones in urinary tract  Bone mineral density (BMD) assessment * At the forearm, hip and spine * Assess degree of bone loss

Answer 24

 Radiological investigations to localize hyperactive or abnormal parathyroid gland * Ultrasound (USG) (Can be intra-operative) * CT scan * MRI * Radioisotope (Thallium,/ Sestamibi) scanning

Answer 25

 Age < 50 years old  Serum total Ca2+: 1 mg/dL above upper limit of normal  24-hour urinary Ca2+ excretion (Hypercalciuria) > 200 mg  Creatinine clearance ↓ by ≥ 30 %  Renal stones  Osteoporosis

Answer 26

 Self-inflammatory disease of the thyroid gland characterized by neck pain or discomfort, tender diffuse goitre and a predictable course of thyroid function evaluation * Also known as painful thyroiditis, subacute granulomatous thyroiditis and subacute non- suppurative thyroiditis * MOST common cause of painful thyroid disease accounting for up to 5% of adult thyroid disease  Family history of subacute thyroiditis * Strongly associated with HLA-B35 or HLA-B67 * Results from a subclinical viral infection that provides an antigen that uniquely binds to HLA-B35 molecules on macrophages * Resulting HLA-B35 complex activates cytotoxic T lymphocytes that damage thyroid follicular cells because the cells have partial structural similarity with the infection- related antigen

Answer 27

NSAID, Steroid Levothyroxine or BB

Answer 28

 Arise from chromaffin cells of adrenal medulla and sympathetic ganglia  Neuroendocrine tumour with serious and potentially lethal cardiovascular complications due to effects of secreted catecholamines

Answer 29

 Arterial supply * Superior adrenal artery (from inferior phrenic artery) * Middle adrenal artery (from aorta) * Inferior adrenal artery (from renal artery)  Venous drainage * Left adrenal vein (drains into left renal vein) * Right adrenal vein (drains into IVC directly)

Answer 30

 Classical triad (Tachycardia + Generalized sweating + Headache)  5Ps of Phaeochromocytoma * Pressure (BP: Sustained or paroxysmal hypertension) * Pallor * Palpitations (Tachycardia) * Perspiration (Generalized sweating) * Pain (Headache/ Chest pain)  Other symptoms * Dyspnea * Tremor * Generalized weakness * Weight loss (hypermetabolism) * Glucose intolerance

Answer 31

* Thyrotoxic periodic paralysis * Hypokalemic periodic paralysis * Hyperkalemic periodic paralysis

Answer 32

>20 years (20-39 years old) Etiology: thyrotoxicosis (any etiology) --> graves disease is the most common cause Precipitating factors: increased adrenaline and insulin release which shifts K+ into cells: stress, heavy excercise, high carbohydrate meals Pathogenesis: thyroid hormone increases NaK+ ATPase activity which drives K+ into cells --> leads ot hyperpolarization of muscle membrane and relative inexcitability of muscle fibers Clinical features: generalized weakness of sudden onset with preserved consiousness: proximal >distal and LL >UL, hypotonia, hyporeflexia, tachycardia, severe arrhythmia (sinus arrest/secondary AV block/VF/VT) Attack frequency: infrequent (interval of weeks to months) Attack period: usually at night or early in the morning, seasonal variation with more frequent attacks in summer months Biochemical features: increased T3 and T4 level, decreased TSH level, increased CK level (rhabdomyolysis), hypoP, HypoMg ECG findings (hypokalemia): sinus tachycardia, ST depression, prolonged QT interval, flattened T wave, presence of U wave, arrhythmia (sinus arrest/ 2nd AV block/VF/VT) K+ during attack: low Acute treatment: K+ supplementation: oral/IV KCl (aware of post treatment rebound hyperK when K+ moves back out of the cells Prevention: IV propranolol (indicated in patients refractory to K+ adminstration). lifestyle modification: low carb diet, refrain from vigorous excercise

Answer 33

Age of onset: 10-20 years old Etiology: **hereditary hypokalemic PP (autosomal dominant)** Precipitating factors: increased adrenaline and insulin release which shifts K+ into cells: stress, heavy excercise, high carb meals Pathogenesis: mutation in gene that codes for alpha1 subunit of Ca2+ channel in skeletal muscles: episodic K+ movement into cells causing weakness. **Mutation in gene that codes for Na+ channel (SCN4A):** anomolous gating pore current that causes aberrant depolarization during attacks of weakness Clinical features: **generalized weakness of sudden onset** with preserved consiousness: Proximal > Distal and LL > UL  **Progressive proximal myopathy, Later onset myopathy**, Eventually develops in majority of patients after age 50 as paralytic attacks subsides, Hyporeflexia/ Areflexia Attack frequency: infrequent (interval of weeks to months) Attack duration: longer (hours-days) Biochemical features: HypoK (during attack but normalize between attacks to distinguish it from secondary hypoK causes), genetic testing, provovative tests: excercise, ACTH administration **ECG (hypoK)**: ST depression, Prolonged QT interval, Flattened T wave, Presence of U wave, Arrhythmia (AF/ SVT/ VF). **EMG: decreased amplitude of CMAP** during attack **K+ during attack: low** (K+ level normalized between attacks except secondary hypoK) Acute treatment: **K+ supplementation** --> Oral/ IV KCl (aware of post-treatment rebound hyperkalemia when K+ moves back out of the cells) Prevention: K+-sparing diuretics -->**Spironolactone**, Carbonic anhydrase inhibitors --> **Acetazolamide**/Dichlorphenamide  Lifestyle modification: Low-carbohydrate diet, Refrain from vigorous exercise

Answer 34

Age of onset: 1-10 years old Etiology: hereditary hyperK PP (autosomal dominant) Precipitating factors: stress, heavy excercise, **fasting**, K+ rich meals Pathogenesis: **mutation in gene that codes for Na+ channel (SCN4A)**: Na+ channel closes too slowly during resting phase, Na+ continues to leak into the muscle cells, leads to oversensitivity and stiffness in the muscels (myotoma) Clinical features: **generalized weakness** of sudden onset with preserved consiousness,** progressive proximal myopathy (later onset myopathy)**, eventually deveops in majority of patients after age 50 as paralytic attacks subside. Hypotonia, myotoma (delayed muscle contraction after contraction) Attack frequency: **frequent** Attack duration: shorter (mins-hours) Biochemical features: **increased K+ level, increased CK level**, genetic testing, provocative tests: excercise, ACTH admin ECG fingins: **peaked T wave (hyperK)**. EMG: electrical myotoma K+ during attack: high/normal Acute treatment: **thiazide diuretics (hydrochlorothiaizide), inhaled B2 agonists: albuterol**, stimulates Na+ K+ pump which increases K+transport into cells (most attacks to not require treatment as they are brief Prevenetion: Thiazide diuretics =**Hydrochlorothiazide**, Inhaled β2-agonist * **Albuterol**, Carbonic anhydrase inhibitors * **Acetazolamide** * Dichlorphenamide  Lifestyle modification: Low-carbohydrate diet, Refrain from vigorous exercise

Answer 35

 Myasthenia gravis (MG)  Botulism  Guillain-Barre syndrome (GBS)  Transverse myelitis  Secondary hypokalemic PP * Thyrotoxic periodic paralysis * Hyperaldosteronism * Renal tubular acidosis o Type I: Distal RTA o Type II: Proximal RTA

Answer 36

 Anti-thyroid drugs or β-blockers * Prevention of thyroid storm  Calcium supplements and vitamin D * Prevention of postoperative hypocalcemia * Prevention of hungry bone syndrome (HBS)  Lugol’s solution * Block iodine uptake and secretion of thyroid hormone * Decrease vascularity of thyroid gland to reduce intraoperative bleeding