Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
81 Cards in this Set
- Front
- Back
|
Char of cretinism and its deficiency.
|
1. Low T4.
2. short stature 3. coarse facial features 4. MR 5. umbilical hernia |
|
|
Precocious puberty results in what morphology/
|
bilateral adrenal cortical hyperplasia.
|
|
|
What enzyme deficiency produces precocious puberty?
|
21-hydroxylase
|
|
|
Following partial thyroidectomy, what levels will be tested?
|
Calcium. Inadvertent removal of parathyroid glands can cause hypocalcemia due to hypoparathyroidism.
|
|
|
name of adrenal cortical adenoma and what is secretes?
|
Conn Syndrome
Aldosterone. Will have decreased renin |
|
|
morpological char of follicular carcinoma
|
1. isolated
2. well-circumscribed nodule with 3. well-differentiated follicles 4. invasion of capsule and blood vessels 5. mets to bone, liver, lung |
|
|
morphological char of Graves disease
|
Diffuse enlargement of thyroid with papillary projections in thyroid follicles and lymphoid aggregates in the stroma
|
|
|
Dx in pt with high and low dexamethasone suppression test with failure to suppress cortisol with either.
|
R/O pituitary adenoma.
Is either ectopic source (lung cancer)with high corticotropin levels or tumor of adrenal cortex withlow corticotropins. |
|
|
Causal agent & name of disease in death of young woman who dies after mild sore throat with enlarged adrenal glands and extensive bilateral cortical hemorrhage.
|
Waterhouse-Friderichsen syndrome.
Neisseria meningitidis. |
|
|
Caused by iodine deficiency.
|
Diffuse nontoxic goiter.
|
|
|
Condition of toxic multinodular goiter in which there is a hyperfunctioning nodule in the goiter.
|
Plummer syndrome.
|
|
|
Dx of pt with painful thyroid enlargement, high T4 that then normalizes after two months.
|
Subacute thryoiditis. May be of viral origin. Transient hyperthyroidism d/t inflammatorhy destruction of the thyroid follicles adn release of TH.
|
|
|
Type of carcinoma assoc with amyloid.
|
Medullary carcinoma. Cancer of parafollicular cells that synthesize calcitonin.
These occur spontaneously in 80% of cases; also part of MEN II and III. |
|
|
char of MEN1
|
1. Pancreas
2. pituitary 3. parathyroid neoplasms/hyperplasia |
|
|
Differentiate b/w 21-hydroxylase and 11-hydroxylase deficiency.
|
Both block cortisol & aldo production, but 21-hydroxylase also blocks production of intermediates with mineralocorticoid activity.
|
|
|
Which genetic mutation is assoc with MEN II?`
|
RET
|
|
|
What conditions associated with MEN II?
|
medullary carcinoma of thyroid.
pheochromocytomas. Parathyroid adenomas. |
|
|
Dx of mass in sella turcica with only prolactin elevation.
|
Hyperprolactinemia is a stalk section effect with loss of inhibiting factor for porlactin.
|
|
|
A destructive sellar mass.
|
Craniopharyngioma.
|
|
|
Most common cause for hypercalcemia
|
Malignancy.
|
|
|
Hashimoto thyroiditis causes what type of antibody titers.
|
Anti-microsomal
Anti-throglobulin. These are present when thyroid enlargement is still present. In burnt-out phase, only hypothyroidism will be detected. |
|
|
Medullary carcinoma is multinodular or singular?
|
Multinodular.
|
|
|
How to test for acromegaly caused by GH-secreting adenoma.
|
Failure to suppress GH levels by glucose infusion.
|
|
|
What does prolactinoma cause?
|
amenorrhea & galactorhea
|
|
|
Signs of chronic adrenal insufficiency.
|
1. Decreased cortisol.
2. Decreased aldo. 3. Hyperpigmentation 4.diarrhea, wt loss 5. increased corticotrophin 6. adrenals show bilateral lymphocytic adrenalitis c cortical atrophy |
|
|
Developmental defect that results in failure of development of 3rd/4th pharyngeal pouches. Lack thymus, parathyroids, clear cells of thyroid.
|
DeGeorge syndrome
|
|
|
Laboratory sign of pheochromocytoma
|
increased urinary free catecholamines, metanephrines and vanillylmandelic acid (VMA)
|
|
|
Mutations in which gene are associated with papillary carcinoma and medullary carcinoma of thyroid?
|
RET protooncogene
|
|
|
Secondary hyperparathyroidism results from
|
Decreased phosphate excretion by kidneys. This depresses calcium, stimulates parathyroid activity.
|
|
|
Characteristics of anaplastic carcinoma
|
Pleomorphic spindle cells.
Mets. Very aggressive |
|
|
Char of papillary carcinoma.
|
Papillary architecture.
Cells with clear nuclei. Irradiation is risk factor. |
|
|
Symptoms of hypercalcemia
|
1. polyuria
2. constipation 3. lethargy 4. disorientation |
|
|
Most common cause of hypercalcemia in hospitalized pt, in outpatient?
|
hospitalized = malignancy
outpt=primary hyperPT |
|
|
adjustment factor for measuring calcium
|
increase Ca by .08 mg/dL for each 1 g increase albumin above 4 gm/dL and vice versa.
|
|
|
Dx of pt with elevated calcium and PTH?
|
Primary hyperparathyroidism.
|
|
|
Most important regulator of parathyroid hormone secretion under physio conditions?
|
Ionized calcium
|
|
|
Other susbstances that affect plasma calcium levels?
|
1. calcitonin
2. 1-25-diOH vit D 3. beta-adrenergic catecholamines |
|
|
Lab values in parathyroid hormone excess
|
1.hypophosphatemia and mild hypercholermic metabolic acidosis d/t urinary loss of phosphate and bicarb
2. hypercaliuria d/t to increased glomerular filtration of calcium. |
|
|
Overall effect of PTH
|
1. resorb bone calcium
2. enhance ca excretion Net loss of total body calcium. |
|
|
2 Long-term clinical effects of elevated PTH
|
1. osteoporosis
2. kidney stones |
|
|
7 Clinical symptoms of hyperparathyroidism that presents rapidly
|
1. weight loss
2. bone pain 3. compression fracture 4. hypercalcemia 5. depression 6. proximal muscle weakness 7. fasciculation of tongue |
|
|
3 manifestations of MEN-I
|
1. Pituitary
2. Parathyroid 3. pancreas |
|
|
3 manifestations of Men IIa
|
1. Medullary thyroid cancer
2. Pheochromocytoma 3. Parathyroid tumor causing increased PTH (only type that causes both thyroid & parathyroid ca). Assoc with RET oncogene |
|
|
3 familial syndromes that can cause hypercalcemia
|
1. MEN-1
2. MEN-IIa 3. Familial hypocalciuric hypercalcemia (FHH) |
|
|
Features of Familial hypocalciuric hypercalcemia syndromne (FHH)
|
Low calcium/creatinine clearance ratio.
High serum Mg++. HYperplasia of all 4 parathyroid glands d/t decreased sensitivity of Ca-sensing receptor |
|
|
Treatment for FHH
|
none. Is mild and non-progressive.
|
|
|
Non-PTH-related hypercalcemia differentials
|
1. malignancy (wt loss, constipation, depression). typically more severe elevation in Calcium.
2. Hyperthyroidism. 3. Addison's disease. 4. Drugs (lithium, thiazide diuretics, antacids, excessive vitamin A and D). 5. Milk alkali syndrome 6. Sarcoidosis, TB, granulomatous fungal disease 7. Rhabdomyolysis 8. Chronic Renal failure 9. immoblization |
|
|
Mneumonic for causes of hypercalcemia
|
VITAMINS TRAP
V - vitamins A and D I - Inflmammation, infection, immobilization T - Thyrotoxicosis or Thiazides A - Addison's disease M - Milk-alkali, medication, myeloma I- above N - Neoplasms S - Sarcoidosis T- above R - Rhabdomylosis or renal failure A - AIDS-related diseases P - Parathyroid overactivity of Paget's disease c immoblization |
|
|
3 ways malignancy may result in hypercalcemia
|
1. osteolytic mets
2. PTH-related protein production 3. Lymphomas that product 1,25-OH vitamin D |
|
|
Treatment of hypercalcemia
|
1. <11.5 mg/dL and asymptomatic: don't treat.
2. mild symptomns: hydrate + non-thiazide diuretics to increase calcium excretion 3. Salmon calcitonin (Miacalcin) 4.IV biphosphonates (pamidronate, zoledronate) 5. Oral phosphate 6. glucocorticoids antagonize GI absorption of calcium. |
|
|
Clinical features of hypocalcemia
|
1. circumoral tingling
2. paresthesias 3. muscle cramps 4. seizures 5. tetany 6. positive Chvostek's or Trousseau's signs 7. lenticular cataracts 8.fungal infections of nails 9. pancreatic calcification 10. prolonged QT interval 11. calcificationof basal ganglia/cerebellar vermis if long-standing |
|
|
What is pseudohypoparathyroidism and what morphology is associated with it?
|
PTH resistance. Presents with Albright's hereditary osteodrystrophy, short stature, obesity, round found, shortening of fingers and toes, subq calcifications, diminished IQ.
|
|
|
What is pseudopseudohypoparathyroidism?
|
Defective Gs protein is inherited from the father, there is no hormone resistance, but are normocalcemic with albrigh's hereditaryh osteodrystrophy.
|
|
|
DDX of hypoparathyroidism.
|
1. Postsurgical
2. Autoimmune 3. idiopathic 4. Hypomagnesemia d/t alcoholism 5. pancreatitits/malabsorption syndrome 6. PTH resistance |
|
|
What may cause factitious hypocalcemia
|
Abnormally low serum albumin.
|
|
|
TX of hypocalcemia
|
1. IV calcium (10% calcium gluconate)
2. Vit D therapy 3. Magnesium replacement if abnormal. |
|
|
What are normal serum calcium levels
|
8.5-9.5 mg/dL
|
|
|
How is calcium found in the serum?
|
50% bound to protein
50% ionized |
|
|
3 ways that PTH affects the kidneys.
|
1. Increased reabsorption of Ca in proximal area
2. Decreased phosphorus reabsorption 3. Increased 1-25 diOH vitamin D synthesis |
|
|
How is Ca linked to Na in kidneys?
|
Na+ and Ca+ move together.
Volume contraction: increased reabsorption of Na and Ca. |
|
|
Source and action of PTH.
|
C cells of thyroid.
Shuts off bone resorption. When Ca is low, PTH is released. As Ca starts to rise, calcitonin is released and shuts off bone breakdown. |
|
|
Lab value for hypercalcemia
|
>10 mg/dl
|
|
|
2 most common causes of hypercalcemia?
|
1. malignancy
2. Hyperparathyroidism |
|
|
Mnenomic for primary hyperparathyrodism
|
bones groans moans stones
|
|
|
IF PTH is high, but 1,25 diOH vitamin D is not elevated?
|
PTH-related protein or ectopic PTH
|
|
|
Hypercalcemia with elevated ACE indicates?
|
sarcoidosis
|
|
|
What is the role of PTH in vitamin D?
|
PTH converts 25-OH vit D tl 1,25-OH vitamin D
|
|
|
What could cause primary hyperparathyroidism?
|
1. 80% = adenoma of parathyroids. (increased gland weight)
2.1-2% parathyroid carcinoma. 3.hyperplasia d/t genetics (FHH), idiopathic, (MEN2A) |
|
|
What is the significance of chloride:phosphate ratio in hypercalcemia?
|
PTH decreases resorption of bicarb and phosphate. Mild acidosis. Since bicarb is lost, Cl must increase. Ratio of cl/phos >33 suggestss primary hyperparathyroidism.
|
|
|
Criteria for surgery for hyperparathyroidism?
|
1. Osteoporosis
2. Ca>12 3. Kidney stones 4. Pancreatitis 5. Ulcer disease 6. Symptomatic 7. renal impairment 8. 24 hr urine is 400 mg 9. Age less than 50 |
|
|
What is the significance of serum magnesium in hypoparathyroidism?
|
Normal Mg needed for proper PTH release, secretion and action.,
|
|
|
How is Mg affected by pernicious anemia?
|
Attacks parietal cells and impairs Mg uptake. b12 def.
|
|
|
Low serum calcium, low phosphorous and elevated alkaline phosphatase indicates what disease?
|
Osteomalacia d/t secondary hyperparathyroidism.
|
|
|
DDX for secondary hyperparathyroidism?
|
1. Vit D deficiency (dilantin and Tegmutol can cause it) Also celiac sprue.
2. chornic renal failure 3. GI malabsoprtive disease 4. Mg depletion 5. Renal leak of Ca. |
|
|
4 DDX for hypocalcemia and elevated PTH.
|
1. Hypomagnesium
2. Renal deficiency 3. Vit D deficiency 4. PTH resistance syndrome. |
|
|
A patient with defective Gs protein may experience resistance to which hormones?
|
PTH
TSH FSH/LH Glucagon ADH |
|
|
DDX for hypercalcemia and increased PTH.
|
1. primary hyperparathyroidism
2. FHH 3. Drugs (lithium, thiazides, Vit D/A toxicity) 4. Renal failure with tertiary hyperparathyroidism |
|
|
TX for FHH
|
none
|
|
|
DDX for hypercalcemia with low PTH.
|
1. Granulomatous disease (sarcoidosis)
2. thiazides 3. Vit A or D deficiency 4. thyrotoxicosis (bone breakdown) |
|
|
How does PTHrp affect PO4?
|
increased renal excretion of PO4.
|
|
|
Cancers associated with PTHrP.
|
1. squamous cell lung ca
2. renal cell ca 3. ca with squamous histology: skin, laryngeal, cervical, vaginal, breat |
