Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Internal Medicine Shelf Exam > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Hyperprolactinemia

A

Clinical:
- pre/menopausal women: oligomenorrhea/amenorrhea + infertility + galactorrhea
-post/menopausal: mass effect symptoms ( headache + visual field defect) —> due to large adenoma
- men: hypogonadism ( decrease libido + erectile dysfunction) + mass effect symptoms ( headache + visual field defect)

Causes:
- physiologic ( pregnancy & breastfeeding)
- chest wall injury ( burns, herpes zoster)
- prolactinoma (pituitary adenoma)
Infiltrative pituitary/hypothalamic disorders ( malignancy or sarcoidosis)
-medication ( antipsychotics, metoclopramide)
- hypothyroidism
- chronic kidney disease

Diagnosis:
- serum prolactin ( usually high)
- MRI of pituitary

Note:
- high prolactin suppress GnRH, LH, estrogen secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Polycystic ovary syndrome (PCOS)

A

Presents with:
- obesity + oligomenorrhea + infertility + signs of hyper/androgenism (hirsutism)
- share similar features as cushing syndrome, except of NO skin atrophy, No muscle weakness, No bruising

Treatment:
- weight loss (first line treatment, to improve fertility)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Primary adrenal insufficiency (PAI) = Addison disease

A

COMBINATION OF:
- increase salt craving + reduced body hair + Major depressive disorder (fatigue, anorexia, memory impairment + lack of motivation + loss of libido)

Caused by:
- bilateral destruction of adrenal cortex

Signs:
1. Mineralocorticoid deficiency: renal salt wasting + hypotension + weight loss + hyponatremia + hyperkalemia + dietary salt craving
2. Glucocorticoid deficiency: fatigue + anorexia + psychiatric signs ( irritability, depressed mood) + hypotension
3. Androgen deficiency: loss of libido + loss of body/pubic hair ( only seen in women due to androgen deficiency; however, in men, testes still produce androgen)

Diagnosis of PAI:
- Via: stimulation testing with cosyntropin (synthetic form of ACTH)
-diagnostic of PAI = low production of cortisol following cosyntropin administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Primary hyperaldosteronism ( Conns disease)

A

Signs:
- hypertension
- hypokalemia ( muscle cramps, weakness, palpitation)
- moist mucus membrane

Diagnosis:
- plasma renin activity & aldosterone concentration

Note:
- patients with mild hyperaldosteronism —> prone to develop diuretic-induced hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diabetic ketoacidosis (DKA)

A

Patient
- young age
- brittle Type 1 DM
- initial manifistation of diabetes

Clinical
-acute to subacute onset
- initial: polydipsia/polyuria + blurred vision + weight loss
- later: altered mental status + hyperventilation +
abdominal pain

Diagnosis
- increase glucose (typically, 300-800 mg/dL) (finger-stick blood glucose monitor)
- metabolic acidosis ( bicarb < 18 mEq/L)
- increase anion gap
- positive serum ketones
- urinalysis shows glucose & ketones

Treatment
1. high-flow IV fluid (normal saline)
2. IV insulin
3. Follow & replace potassium

Approach:

  1. Hydration to restore Intravascular volume, with 0.9% (normal) saline recommended in the first 1-2
  2. Correction of hyperglycemia & ketosis with IV regular insulin
  3. Serial assessment of electrolytes, especially potassium
  4. Treatment of the underlying precipitating factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cushing syndrome vs. disease

A

Cushing syndrome:

caused by:
-exogenous administration of glucocorticoid
- ACTH-producing pituitary tumor (Cushing disease) ( ACTH-dependent cause)
- ectopic ACTH production (small cell lung cancer) ( ACTH-dependent cause)
-primary adrenal disease ( ACTH- independent cause)

Note:
-myopathy in cushing syndrome is characterized by progressive painless muscle weakness predominantly involving the proximal muscles. It is due to the direct catabolic effects of cortisol on skeletal muscle, leading to muscle atrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Primary adrenal insufficiency

A

Mechanism
- destruction of adrenal cortex

Etiology:
- autoimmune adrenalitits
- infection, malignancy

Findings:
Cortisol (low)
Aldosterone (low)
ACTH (high)

Symptoms:
- severe symptoms
- hypovulemia
-hyponatremia
-hyperkalemia
-hyperpigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Secondary adrenal insufficiency

A

Mechanisms:
- disruption of hypothalamic-pituitary axis

Etiology:
- glucocorticoid therapy
-infiltrative diseases

Findings:
- aldosterone (normal)
- cortisol (low)
- ACTH (low)

Symptoms:
- mild symptoms
- euvolemia
-minimal electrolytes disturbance
- no hyperpigmentation

Symptoms:
- weakness, abdominal pain, loss of appetite,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hyperthyroidism —> thyrotoxicosis with normal or increase RAI

A

-caused by: overproduction of thyroid hormone

Seen with:
- graves disease (stimulation of TSH receptor by thyrotropin-receptor antibody) —> ( suppress TSH, thyroid gland is enlarged)
- toxic multi-nodular goiter
- toxic nodule

Treatment:
- Methimazole ( to decrease overproduction of thyroid hormones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hyperthyroidism —> thyrotoxicosis with decrease RAIU

A
  • caused by: release of preformed hormones

Seen with:
1. painless (silent) thyroiditis —> signs ( painless + enlarged+ non-tender goiter) + associated with thyroid peroxidase antibodies + a variant of lymphocytic (Hashimoto) thyroiditis + similar to postpartum thyroiditis (except that it exclude patients within a year of pregnancy) + no need for therapy + beta-blocker to control symptoms ( palpitation, tremors)

  1. subacute ( de Quervain) thyroiditis —> treat with prednisone ( to reduce thyroid pain), if not responding to NSAIDs + signs ( painful + enlarged+ tender goiter) + precedded by Upper respiratory tract infection
  2. amiodarone- induced thyroiditis —> treat with prednisolone ( especially type 2; destructive thyroiditis)
  3. excessive dose of levothyroxine
  4. struma ovarii
  5. iodine-induced
  6. extensive thyroid cancer metastasis

Note:
- primary hyperthyroidism = suppress TSH + increase T4 + signs of thyrotoxicosis ( tachycardia, anxiety, weight loss)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cushing syndrome

A

Signs:
- proximal muscle weakness —> muscle atrophy
- nocturnal muscle cramps
- weight gain
- bruising
- hypertension
- dark upper lip hair
- face acne
- tinea versicolor on the trunk ( fungal infection)
- hyperpigmentation ( with ACTH- dependent Cushing syndrome
- hyperandrogenism ( menstrual irregularity + face acne + hirsutism)

Signs:
- moon faces
- muscle wasting
- striae
- supra-clavicular fat pad
- dorsocervical fat pad (buffalo hump)
-bruising
-central obesity

Laboratory:
- normal platelet + normal anticoagulation = even with bruises
-hyperglycemia
- hypokalemia
-metabolic alkalosis

Diagnosis:
1. hypercortisolism ( late-night salivary cortisol assay, 24 hours urine free cortisol measurement, overnight low-dose dexamethasone suppression test)

  1. ACTH level
    - ACTH-dependant ( ACTH-secreting pituitary tumor, ectopic ACTH)
    - ACTH- independent (adrenal adenoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Milk - alkai syndrome

A
  • seen with osteoporosis patient taking excessive calcium & absorbable alkali ( calcium bicarbonate)
  • findings:
    1. Symptomatic hypercalcemia
    2. Metabolic alkalosis
    3. Acute kidney injury
    3. Suppressed PTH
    4. Polyuria/polydipsia
    5. N/V, constipation

TREATMENT:
- discontinue causative agent
- isotonic saline followed by furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Vitamins:

A

Vitamin A:
- excessive dose leads to bone turnover, abdominal pain, hypercalcemia, dry skin, headache, blurry vision

Vitamin C:
- deficiency: causes microvascular bleeding

Vitamin K:
- deficiency: causes bleeding, reduce coagulation factors ( 2,7,9,10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of hirsutism in women

A
  1. PCOS:
    - Oligomenorrhea + hyperandrogenism + obesity
    - associated with type 2 diabetes + dyslipidemia + HTN
    - high Testosterone & LH, normal DHEAS
  2. Cushing syndrome:
    - oligomenorrhea + obesity ( face, neck, trunk, abdomen)
    - increased libido + virilization (male/female characteristics)
    -
  3. Idiopathic hirsutism:
    - normal menstruation
    - normal androgen level
  4. Non-classic 21-hydroxylase deficiency:
    - similar to PCOS
    - Elevated serum 17-hydroxy- progesterone
  5. Androgen-secreting ovarian tumor; ovarian hyperthecosis
    - more common in post-menopausal women
    - rapidly progressive hirsutism with viralization
    -very high serum androgen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Women and androgens production

A

Women produce:

  • testosterone & DHEA: from ovaries & adrenal
  • DHEAS: from adrenal gland

Notes:
- most androgen-producing adrenal tumor overproduce —> DHEAS
—> high DHEAS & testosterone
—> low LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Euthyroid sick syndrome

A
  • due to decrease PERIPHERAL conversion of T4 to T3
  • Can be caused by: high cortisol level, glucocorticoid use, acute illness

Signs:
- normal TSH & T4
- low T3
- High reversed T3
- lead to transient hypothyroidism state

Notes:
Seen in:
- in some settings ( Ulcerative colitis with hematochezia, diarrhea, abdominal pain, fever)

  • T4 produced in thyroid; T3 produced peripheral via deionization of T4 —> T3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of graves hyperthyroidism

A
  1. Antithyroid drugs:
    - PTU ( 1st trimester pregnancy) + methimazole
    - in mild hyperthyroidism
    - older patients
  2. Radioactive iodine (RAI)
    - in moderate hyperthyroidism +/- proptosis
  3. Thyroidectomy
    - severe hyperthyroidism
    - large goiter (suspect for cancer)
    -pregnancy (cant take thioamides)
    -severe opthalamoplegia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Two important causes of hypoglycemia in non-diabetic patients with elevated insulin levels?

A

Signs of hypoglycemia:
- palpitation + tremor + nervous + headache + sweaty + shaky

Hypoglycemia + elevated insulin, seen in:
1. Insulinoma (beta cell tumors)
2. Surreptitious use of insulin or sulfonylurea

Note:
- elevated C-peptide levels & proinsulin levels (greater than 5) are seen in patients with beta cell tumors

  • patients with non-beta cell tumor ( large mesenchymal tumors) —> have hypoglycemia independent of insulin —> have elevated IGF II levels, suppressed insulin, suppressed c-peptides
  • sulfonylurea —> high endogenous insulin, high C-peptides ( differentiate from insulinoma by measuring sulfonylurea level)
  • exogenous insulin —> high serum insulin, low C-peptides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Glucose & insulin

A
  • glucose level of < 60 —> does not allow for insulin secretion
    ( hypoglycemia leads to suppression of insulin)
  • in a case of hypoglycemia & increase insulin ( insulinoma & use of insulin or sulfonylurea) —> elevated C-peptides & proinsulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Scenario of DIABETIC INSIDIOUS

A
  • polydipsia/dysuria + obesity + hypernatremia + acute kidney injury ( decrease renal perfusion due to volume overload) + hyperurecemia + increase serum osmolality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ADH- related causes of polyuria & polydipsia

A

Primary polydipsia:
- increase water intake
- anti-psychotic + anxious + middle age woman
- low serum Na
- diluted urine ( urine osmolality < 1/2 serum osmolality)
- hyponatremia (<137)

Diabetic insipidus:
- reduce ADH release from pituitary
- idiopathic + trauma + pituitary surgery + ischemic encephalopathy
- high serum Na
-diluted urine

Nephrogenic Diabetic insipidus:
- normal ADH level with varying resistance in kidney
- chronic lithium use + hypercalcemia + hereditary ( AVPR2 mutation)
- normal serum Na

Others:
- diabetic patient also have polydipsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diabetic insipidus (central)

A

Signs:
- polyuria + diluted urine ( urine osmolarity < 275)
- polydipsia ( increase water intake)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
A

HYPONATREMIA
HYPERKALEMIA
HYPOTENSION
DECREASE BICARB = ACIDOSIS ?
INCREASE CREATININE
HYPERGLYCEMIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Addison disease (primary cause of adrenal insufficiency)

( also, autoimmune adrenalitits)

A
  • not enough cortisol & aldosterone produced
  1. Autoimmune disease
  2. Drugs (ketoconazole, rifampin)
  3. Destruction of adrenal gland ( trauma, hemorrhage, metastasis)
  4. Infection (TB, HIV)
  5. Skin changes (hyperpigmentation due to increase ACTH)
  6. Orthostatic hypotension ( volume depletion & reduced vascular tone)
  7. Hyponatremia (low Na), hyperkalemia ( high K)
    —> due to renal sodium loss & increase secretion of ADH
    —> due to renal potassium retention
  8. Acute adrenal crisis ( confusion/ hypotension/shock)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Secondary Adrenal insufficiency
( failure of pituitary gland to produce ACTH)

A
  • lack of cortisol, but aldosterone is ok

( caused by alcohol, infection, pregnancy, fasting)

  • most common cause is Exogenous glucocorticoid use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Symptoms of primary & secondary causes of adrenal insufficiency

A

Primary & secondary causes:
1. Anorexia, N/V, salt craving, hypoglycemia ( due to lack of cortisol)

Specific for Addison disease:
1. Hyperpigmentation ( due to increase ACTH)
2. Orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Diagnosis & treatment of adrenal insufficiency

A

Diagnosis:

  • 8 am high-dose ACTH (Cosyntropin)
    1. No/low cortisol produce —> addision disease (due to destruction of adrenal gland)
    2. If cortisol is elevated —> secondary cause

Treatment:

  1. Primary cause —> hydrocortisone + fludrocortisone (similar to aldosterone, regulates BP & Na)
  2. Secondary —> hydrocortisone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Cushing syndrome

A
  1. Excess cortisol production

Caused by:
1. Long-term use of glucocorticoid
2. Increase ACTH production from pituitary gland hyperplasia/adenoma —> Cushing disease
3. ACTH-producing tumor ( small cell lung cancer)
4. Adrenal tumor leading to increase cortisol

Symptoms:
1. Obesity, HTN, oily skin, acne, hirsutism, moon faces, buffalo hump, thin extremities, striae, acanthosis nigricans, hyperpigmentation (if increase ACTH)

Diagnosis:
1. 24 hours urine free cortisol (most common)
2. Nighttime salivary cortisonl
3. Overnight Low-dose Dexamethasone suppression test
—> if cortisol increase & not suppressed (Cushing syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Laboratory test to differentiate etiology of Cushing syndromee

A
  • get baseline of ACTH + high-dose Dexamethasone suppression test
  1. If Cushing disease (pituitary hyperplasia/adenoma)—> high ACTH + suppression of cortisol
  2. If ectopic ACTH-producing tumor —> high ACTH + no suppression of Cortisol
  3. If adrenal tumor —> low ACTH + no suppression of cortisol

Treatment:
1. Taper gradually, if from exogenous steroid
2. Trassphenoidal resection, if from Cushing disease
3. Surgical removal (+ ketoconazole), if from adrenal or ectopic tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Primary hyperaldosteronism (HTN, hypokalemia, metabolic alkalosis, mild hypernatremia) —> Conn Syndrome

& aldosterone escape ( limits edema)

(Diagnosis confirmed by low plasma renin & high serum aldosterone)

A
  1. Bilateral nodular hyperplasia
  2. Hyperfunctioning adrenal adenoma

Lead to:
1. High aldosterone
2. Low potassium reabsorption (hypokalemia)
3. Low H reabsorption (metabolic alkalosis)
4. High Na reabsorption (hypertension/increase blood volume) —>

Aldosterone escape ( limits edema)
- low renin & low angiotensin 2
- high renal blood flow, high GFR, high ANP —> high Na excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Symptoms, Diagnosis, treatment of primary hyperaldosteronism ( Conn syndrome)

A

Signs:
1. High aldosterone, low potassium reabsorption, low H reabsorption, high Na reabsorption, low renin, low angiotensin 2

Symptoms:
1. HTN, hypokalemia, mild hypernatremia, metabolic alkalosis + no significant peripheral edema due to aldosterone escape

Diagnosis:
1. Elevated serum aldosterone & low plasma renin ( aldosterone/renin ratio > 20)
2. Adrenal suppression testing after oral sodium load
3. CT scan & adrenal venous sampling ( to distinguish between unilateral adenoma & bilateral hyperplasia)

Treatment:

Unilateral adenoma:
1st line: Surgery
2nd line: Spironolactone or eplerenone (aldosterone antagonist) —> if surgery is not tolerated

Bilateral hyperplasia:
1st line: Spironolactone or eplerenone ( aldosterone antagonist)
2nd line: potassium-sparing diuretics (amiloride, triamterene) —> if aldosterone antagonist is not tolerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Addison disease (primary adrenal insufficiency)
vs.
Conn disease ( primary hyperaldosteronism)

A

Addision disease:
1. Hyponatremia + hyperkalemia

Conn disease
2. Hypernatremia + hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hypothalamic pituitary thyroid axis

A
  1. Hypothalamus —> release (Thyrotropin-releasing hormone) ( TRH)
  2. Anterior pituitary gland —> release TSH or prolactin
  3. Thyroid gland —> TSH regulates the amount of T4 produced & T4 turns into its active form of T3 in the peripheral tissue ( liver)

—> amount of thyroid hormones produced -> negative effect on TSH & TRH

34
Q

Hashimoto thyroiditis

(hypothyroidism)

A
  • women 30-50
  • autoimmune destruction of thyroid cells by:
  1. Thyroglobulin antibodies
  2. Antithyroid-peroxidase

Symptoms:
1. Weight gain, cold intolerance, dry skin, hoarseness, constipation
2. bradycardia, decrease DTR (Achilles’ tendon) ( decrease relaxation), loss out outer 1/3 of eyebrows, myxedema (non-pitting edema)

Diagnosis:
1. Increase TSH + decrease free T4 or decrease free T3
2. Positive antithyroid peroxidase &/or anti-thyroglobulin antibodies
3. Radioactive uptake scan —> will show diffuse decrease iodine uptake
4. Biopsy —> shows Hurthle cells (Askanazy cells)

Treatment:
1. Levothyroxine (synthetic T4) (synthroid)
—> monitor every 6 weeks
—> NPO 30-60 min before medication
—> 4 hour gaps from PPI, iron, calcium supplement

35
Q

Graves disease

(Hyperthyroidism)

A
  • autoimmune disease
  • TSH receptor antibodies attack & activates TSH receptor leading to increased thyroid hormone

Symptoms:
1. Increased Thyroid hormone
2. Palpitation, weight loss, heat intolerance, atrial fibrillation, graves opthalmopathy (proptosis, exophthalmos, lid lag)
3. Peritibial myexedema (red/brown rash on lower legs with non-piting edema)
4. Enlarged, non-tender thyroid
5. Thyroid bruit

Diagnosis:
1. Decrease TSH, increase free T4 or increase free T3
2. TSH receptor antibody ( thyroid stimulating immunoglobulin)

Treatment:

  1. Radioactive iodine ablation (can worsen opthalmopathy & lead to hypothyroidism state)
  2. Thyroidectomy ( lead to permenant hypothyroidism & laryngeal nerve palsy)
  3. Methimazole (blocks production of new T4 to T3)
    —> can lead to agranulocytosis (patient developing sore throat or fever, should stop the drug)
  4. PTU —> block conversion of T4 to T3
    *** PTU has a black box warning for —> hepatotoxicity & ANCA-associated vasculitis
    —> can lead to agranulocytosis (patient developing sore throat or fever, should stop the drug)

(PTU: used in 1st trimester of pregnancy, methimazole used in 2nd & 3rd trimester of pregnancy)

  1. Beta blocker —> reduce tremor, palpitation, A.fib
  2. Steroid for opthalmopathy
36
Q

Thyrotoxic crisis
(Thyroid storm)

(Hyperthyroidism crisis)

A
  • occurs in untreated/partially treated hyperthyroid patients, usually after surgery, infection, trauma, or other stressful event

Symptoms:
1. Hyper-metabolic state
2. Tachycardia, fever, CNS dysfunction, afib

Diagnosis:
1. Decrease TSH (often undetected), increase free T4/T3

Treatment:
1. IV fluid
2. Beta-blocker (propranolol)
3. PTU > methimazole
4. Glucocorticoid
5. Antipyretic (NSAIDs, avoid aspirin), cooling blanket

37
Q

Myexedema Coma

(Hypothyroidism crisis)

A

-extreme form of hypothyroidim

  • elderly + women + in winter months
  • acute precipitating factors ( CVA, infection, noncompliance with medication)

Diagnosis:
- increase TSH, Decrease T4/T3

TREATMENT:
- IV levothyroxine
- supportive: passive warming, IV fluid

38
Q

Painful thyroid found in

A
  • suppurative thyroiditis
  • subacute thyroiditis
39
Q

Suppurative thyroiditis

A
  • infection of the thyroid from either:
    1. Gram (+) or Gram (-)
    2. Most common Staph. Aureus

Symptoms:
1. Painful thyroid
2. Fever, chills, over malaise
3. Normal thyroid function & hormones (Euthyroid patient)

Diagnosis:
1. Leukocytosis
2. High ESR
3. FNA (to culture & diagnosis the type of organism)
4. Thyroid function test is usually normal

Treatment:
1. Antibiotics
2. Drainage of abscess

40
Q

Subacute thyroiditis ( Dequervain or Granulomatous)

A
  • idiopathic or follow a viral infection (URI last week…)
  • hyperthyroid initially, then euthyroid, then hypothyroid, then back to euthyroid
  • symptoms:
    1. Painful thyroid
    2. Maybe accompanied by URI symptoms

Diagnosis:
1. Increase ESR
2. Hyperthyroid lab (if early on)
3. Biopsy: multinucleate giant cells

Treatment:
1. Supportive ( will eventually go back to euthyroid state)

41
Q

Subclinical hypothyroidism

(Asymptomatic patient with increase TSH)

A
  • normally asymptomatic patient + abnormal thyroid function lab ( increase TSH + normal T4/T3)

Treatment:
1. Observation in most cases (resolve in 6 months)
2. If TSH > 10, treat with low dose levothyroxine to avoid cardiovascular complication

42
Q

Euthyroid sick syndrome (ESS)

A
  • Really sick + old patient + with precipitating event ( MI, sepsis, malignancy)
  • the underlying illness, lead to decrease conversion of T4 to T3

Diagnosis:
1. Decrease T3

Treatment:
1. Treat underlying cause

43
Q

Postpartum thyroiditis

A
  1. Low TSH, high T4/T3
  2. High thyroglobulin
  3. Low radioiodine uptake
  4. Positive thyroid peroxidase antibody
  5. Negative thyrotropin receptor antibody

Treatment:
1. Hyperthyroid phase —> beta-blocker
2. Hypothyroid phase —> levothyroxine
3. Euthyroid phase —> wean of levothyroxine & measure TSH every year

44
Q

Thyroiditis

A
  1. Hashimoto ( autoimmune thyroiditis)
    —> diffused goiter
    —> hypothyroid phase
    —> positive TPO, variable radioiodine uptake
  2. Silent/painless thyroiditis
    —> small, nontender goiter
    —> hyperthyroid phase
    —> TPO positive, low radioiodine uptake
    —-> note : different than Graves disease ( shows high radioiodine uptake)
  3. Subacute (de-queverien ) thyroiditis
    - post viral infection
    - predominant hyperthyroidism + fever
    - painful/tender goiter
    - elevated ESR/CRP
    - low radioiodine uptake
45
Q

Evaluation of thyroid nodule

A

Start with:
1. TSH level
2. Ultrasound of thyroid

Normal OR elevated TSH:
1. FNA & biopsy

Low TSH —> Radioactive iodine scintigraphy
1. Cold nodule ( hypofunction) —> FNA & Biopsy
2. Hot nodule (hyperfunction) —> treat hyperthyroidism

46
Q

High titers of anti-TPO

A
  • increased risk of miscarriage in both euthyroid & hypothyroid women
47
Q

TSH- secreting pituitary adenoma

(Secondary hyperthyroidism)

A
  • increase TSH, increase T4/T3
  • MRI for Pituitary glad
48
Q

Evaluation of hyperthyroidism

A

Measure serum TSH, T4, T3

  1. Primary hyperthyroidism
    - low TSH, high T4/T3
    - Signs of graves disease ( goiter, ophthalmology)
    1.. yes—> graves disease
    2..No —> radioactive iodine uptake:
    —> high:
    1. Diffused goiter: graves disease
    2. Nodular goiter: toxic adenoma or multinodular goiter—> low: Measure serum thyroglobin
    1. Low: exogenous hormone
    2. High: thyroditis or iodine exposure

Secondary hyperthyroidism:
- High TSH, high T4/T3
- MRI of pituitary gland
- macroadenoma ( + mass effect: headache, visual field defect)

49
Q

Drugs for neuropathic pain ( burning & stabbing pain in feet ) in diabetic patients

A

Initial treatment of painful diabetic neuropathy is:

  1. Amitriptyline (Tricyclic antidepressant) (age < 65)
  2. Duloxetine (SNRI)
  3. Gabapentin/pregabalin (anticonvulsant) (age > 65)
  4. Opioid
  5. Topical capsaicin
  6. Lidocaine
50
Q

Assess foot (neuropathic) ulcer in patients with diabetes

A
  • assess with: monofilament test (predict risk for future ulcer)
  • most common cause for foot ulcer is diabetic neuropathy (decrease pain sensation & pressure perception —> lead to muscle imbalance —> lead to foot deformities & impairs the microcirculation & integrity of the skin)
  • neuropathic ulcer occurs underneath bone prominence in the feet

Others:
1. Decrease vibration sensation ( tuning fork)
2. Decrease pinprick sensation
3. Decrease temperature sensation

51
Q

Diabetic neuropathy

A
  • decrease sensation, vibration, pinprick, temperature sensation
  • usually absent ankle reflex
  • knee reflex not affected
52
Q

Diabetes type 1

(No insulin production)

A
  • caused by pancreatic beta cell destruction, the pancreas is no longer making insulin
  • patient are usually < 30 years of age at time of diagnosis

Etiology:
1. Type 1A: autoimmune
—> positive GAD antibodies, islet cell antibodies

  1. Type 1B: non-autoimmune beta cell destruction
    —> idiopathic. Strong hereditary component

Symptoms: (pee, drink, eat alooot)
1. Polyuria, polydipsia, polyphagia
2. DKA (if blood sugar get high)

Diagnosis:
1. Fasting plasma glucose > 126 (on two separate occasions)
2. 2 hour glucose tolerance test > 200
3. A1C of > 6.5%
4. Or random blood glucose of > 200 in symptomatic patient (polydipsia, polyuria, polyphagia)

Treatment:
1. Insulin:
2. Fast acting —> Lispro, Aspart ( 5-15 min onset) (meal time insulin)
3. Intermediate —> NPH ( 2 hour onset)
4. Long acting/basal —> determir, Glargine ( 12-24 hr insulin)

53
Q

Somogyi phenomenon

A
  • overnight hypoglycemia, followed by rebound hyperglycemia

—> low blood glucose overnight causes a surge of hormones to try to compensate, causing insulin resistance in the morning hours

54
Q

Dawn phenomenon

A

Overnight surge of hormones from overnight-fast leads to hyperglycemia (2-8 am)

55
Q

Type 2 diabetes

(Produce insulin, resistance)

A
  • insulin resistance combined with impaired insulin secretion

Risks:
- obesity
- genetic & environment

Symptoms:
1. Polydipsia, polyphagia, polyuria
2. Poor wound healing, yeast infection, UTI

Treatment:
1. Initially, life style changes
2. Metformin
3. SGLT2- inhibitor
4. GLP-1 agonist
5. Sulfonylurea

56
Q

Diabetic ketoacidosis

(Acute presentation)

A
  • common in type 1 diabetes

Etiology: (5i)
1. Infection ( UTI, pneumonia, septic)
2. Iatrogenic ( corticosteroid)
3. Infarction ( MI, CVA)
4. Ignorance ( not adherent to medication)
5. Infant on board (pregnancy)

Symptoms:
1. N/V, abdominal pain
2. Polyuria, polydipsia
3. Fruity (acetone) breath
5. Dehydration (tachycardia & tachypnea)
6. Kussmaul respiration (deep heavy exhalation/expiration)

Diagnosis:
1. Blood sugar > 250
2. Arterial pH < 7.30 & bicarb < 22 ( metabolic acidosis with high anion gap)
3. Positive ketone in urine

Treatment: (SIPS of water)
1. Saline
—> isotonic at first, then once blood glucose < 250, change to dextrose 5%

  1. Insulin
    —> regular insulin (but no insulin given, if potassium < 3.3)
  2. Potassium supplement
    —> don’t give potassium if it is > 5.3 at admission. ( it is safe to assume that all patient with DKA are total body potassium deficient (even if lab says otherwise)
  3. Search for underlying cause ( 5i’s: infection, iatrogenic, infarction, ignorance, infant of board)
57
Q

Hyperosmolar hyperglycemic state

( slower at onset, over days)

A
  • common in type 2 diabetes

Etiology:
- same as DKA: infection, iatrogenic, infarcts, ignorance, infant on board

Patho:
1. Illness or stress causes lack of fluid intake —> leading to severe dehydration —> ultimately, leading to increased serum osmolality, hyperglycemia, hypokalemia

Symptoms:
1. N/V, abdominal pain
2. Polyuria, polydipsia
3. Altered mental status (confusion)

Diagnosis:
1. Blood sugar > 600
2. Increased osmolality > 320
3. Absence of acidosis ( pH > 7.30) (normal pH, normal bicarb)
4. Normal anion gap
5. No/small serum ketone

58
Q

Uncontrolled diabetic type 2 & cardiovascular disease

A
  • benefit from:
    1. Glucagon-like peptide-1 receptor agonist ( GLP-1 agonist)
    2. SGLT2-inhibitor

—> both lead to weight loss

59
Q

Diabetic gastroparesis ( delayed gastric emptying) present in the setting of poor glycemic control

A
  • treated with —> metoclopramide
60
Q

Primary hyperparathyroidism

A

—> hypercalcemia ( polyuria, kidney stone, decrease bone density)

—> hypophosphatemia

61
Q

MEN type 1

A

All lead to hypercalcemia & recurrent peptic ulcer:

  1. Primary hyperparathyroidism
    —> hypercalcemia (polyuria, kidney stone, low bone density)
  2. Pituitary adenoma
    —> hormone secretion ( ACTH, GH, Prolactin) + mass effect (headache + visual deficit)
  3. GI/pancreatic endocrine tumor (gastrinoma)
    —> gastrinoma (recurrent peptic ulcer)
    —> insulinoma ( hypoglycemia)
    —> Vipoma (secretory diarrhea, hypokalemia, hypochlorhydia)
    —> glucangoma (weight loss, necrolytic migratory erythema, hyperglycemia)
62
Q

Medullary thyroid cancer is a calcitonin-producing tumor of the thyroid parafollicular C cells

A
  • occurs as component of MEN type 2A & 2B
  • associated with pheochromocytoma
  • patient with Medullary thyroid cancer should be screened for pheochromocytoma prior to thyroidectomy with plasma fractionated metanephrine assay
63
Q

Chronic pancreatitis or pancreatic resection

A
  • associated with pacreatogenic diabetes:
  1. Loss of insulin producing beta cells
  2. Loss of glucagon-producing alpha cells
  • at risk for rapid & severe hypoglycemia ( sweating, palpitation, tremor)
64
Q

ADH (Hormone)

( increase plasma osmolality —> increase ADH release —> increase water reabsorption)

A
  1. Antidiuretic hormone —> arginine vasopressin
  2. Produced by the posterior pituitary gland
  3. Response to plasma osmolality level

Example:
Increase plasma osmolarity —> indicates decreased blood volume ( dehydration) —> posterior pituitary secretes ADH to signal the kidney to conserve & absorb more water

65
Q

Serum osmolarity

A

Low osmolarity —> Large blood volume ( low solutes)

High osmolarity —> low blood volume ( due to many solutes)

66
Q

Syndrome of inappropriate antidieritic hormone ( SIADH)

( lead to hyponatremia —> due to absorption of water)

A
  1. Body producing higher than normal ADH —> body retaining free water —> leading to hyponatremia (cerebral edema)

Causes:
1. CNS: subarachnoid hemorrhage, CVA, head trauma
2. Small cell lung cancer
3. Anticonvulsant ( carbamazepine)
4. Hydrochlorothiazide
5. SSRI
6. TCA

Symptoms:
1. Altered mental status
2. Coma
3. Seizure

Diagnosis:
1. Normovolemic, hypotonic (low solute conc.), hyponatremia
2. Low serum osmolality
3. High urine osmolality (concentrated urine)
4. High ADH level

Treatment
1. Treat underlying cause
2. Mild: water restriction
3. Moderate: vasopressin receptor antagonist (Tolvaptan) (ADH receptor antagonist)
4. Severe: IV hypertonic saline, furosemide
5. Chronic cases: Demeclocycline (tetracycline derivative)

67
Q

Diabetes insipidus

(Polydipsia +polyuria + mild hypernatremia + increase serum osmolality + decrease urine osmolality)

A
  1. Kidney is unable to reabsorb water due to low ADH secretion or kidney can’t respond to ADH leading to large volume of diluted urine being excreted
  2. Types:
    - central:
  3. Most common type
  4. Pituitary is not releasing ADH
  5. Caused by: idiopathic, head trauma, pituitary destruction
  • nephrogenic:
    1. ADH is being released by pituitary, but the kidney are not responsive to the hormone
    2. Causes: Lithium, electrolyte imbalance, hypokalemia, hypercalcemia

Symptoms:
1. Polyuria + polydipsia
2. Altered mental status (from hypernatremia)
3. Dry mucous membrane, hypotensive

Diagnosis:
1. Increase serum osmolality ( concentrated serum)

  1. Decrease urine osmolality ( diluted urine)
  2. Fluid depravation test:
    - deprive patient for 8 hours
    - normal people: urine will become concentrated
    - DI patient: urine will remain diluted ( < 300 mOsm)
  3. Differentiate between central or nephrogenic DI:
    - Desmopressin (synthetic ADH) stimulation test:
    • central DI: response to ADH & urine output reduces & becomes more concentrated
    • nephrogenic DI: does not response to ADH, diluted urine persist

TREATMENT:
1. Central DI:
- ADH (desmopressin)

  1. Nephrogenic DI:
    - treat underlying cause ( medication or electrolyte imbalance)
    - use hydrochlorothiazide,
68
Q

Hyperparathyroidism ( primary)

A
  • excessive PTH relase
  • caused by:
    1. Parathyroid adenoma
    2. MEN 1 & 2A
    3. Lithium

Symptoms:
1. Asymptomatic
2. Hypercalcemia: (< 14)
- bone ( osteitis fibrosa cystica, osteoporosis)
- kidney stone
- abdominal pain, N/V, constipation
- depression, lethargy…
- decrease DTR

Diagnosis:
- TRIAD OF —> high Ca + low PO4 + high PTH
- 24 hour urine calcium collection ( shows increased urine Ca)

Treatment:
1. Parathyroidectomy
2. Vitamin D & Ca supplementation post parathyroidectomy
3. If patient is not candidate for parathyroidectomy —> use Cinacalcet ( inhibits PTH)
4. If severe cases: Iv hydration +furosmide

69
Q

Hypoparathyroidism

A

Caused by:
1. Post thyroidectomy
2. Hashimoto thyroiditis ( autoimmune)

Symptoms:
1. Periorbital numbness
2. Chvostek sign ( tap cheeks gets spasm)
3. Trousseau sign ( carpopedal spasm with BP cuff)
4. Tetany

Diagnosis:
1. Triad of: low Ca + high Po4 + low PTH
2. ECG: prolonged QT interval

Treatment:
1. Calcium + vitamin D supplement
2. Severe cases: Iv calcium gluconate

70
Q

Refeeding syndrome

A
  1. Carbohydrate intake —> stimulates insulin activity —> promotes cellular uptake of phosphorus, potassium, magnesium —> leads to electrolyte imbalance
  2. Cardiac manifistation ( arrhythmia + CHF) + muscular weakness/rhabdomyolysis + GI ( diarrhea, elevated ALT/AST) + tremor/seizure
71
Q

Hypercalcemia (> 14 ) seen with malignancy

A
  • caused by high PTHrP & low PTH
72
Q

Hypoglycemia occurs in patient with severe illness ( & without history of diabetes)

A
  • due to increase tissue glucose use & suppression of gluconeogenesis in the liver
73
Q

Hyperandrogenesim in women

A
  1. PCOS
  2. Congenital adrenal hyperplasia
    - deficiency in 21 —> lead to production of 17
  3. Ovarian/ adrenal tumor:
    - hirsutism + temporal balding + excessive muscular development + enlarged clitoris —> all less than a year
    - check for testosterone & DHEA levels
    1. High testesterone & normal DHEA —> suggest ovarian tumor
    2. High DHEA —> suggest adrenal tumor
  4. Hyperprolactinemia
  5. Cushing syndrome
  6. Acromegaly
74
Q

Hypopituitary

A

Triad of:
- glucocorticoid deficiency + hypogonadism + hypothyroidism

75
Q

Anorexia nervosa

A

Complication:
1. Hypotension
2. Bradycardia
3. Edema
4. Gastroparesis
5. Cardiac atrophy
6. Decrease bone mineral density

76
Q

Vitamin D deficiency or chronic kidney disease —> lead to hypocalcemia & high PTH

A
  • Measure serum 25-hydroxyvitamin D level
77
Q

Clinical evaluation of acromegaly

(Excessive secretion of GH due to pituitary adenoma)
(

A
  1. Elevated Insulin-like growth factor -1
  2. Oral glucose suppression test
  3. Inadequate GH suppression
  4. MRI of the brain (pituitary mass or normal pituitary)

Diagnosis:
1. Elevated IGF-1
2. ECHO: concentric LV hypertrophy & diastolic dysfunction

Treatment:
1. Transphenoidal resection of pituitary adenoma

78
Q

Oral estrogen replacement therapy in elderly women (post-menopausal )

A
  1. increase in thyroxine-binding globulin (TBG) —> lead to decrease free thyroid hormone levels
  2. Patient with hypothyroidism & levothyroxine therapy —> are unable to increase endogenous thyroid hormone production to compensate —> and require an increased levothyroxine dose
79
Q

Hypovolemic hyponatremia

A
  1. Hypovolemia: diarrhea, poor skin turger, hypotension, low renal perfusion

Low renal perfusion —> stimulated RAAS system —> increase renin, increase aldosterone —> this, stimulates ADH to reabsorb sodium & water at distal tubule

80
Q

Cardioeversion

A

Used in ventricular tachycardia + hypotension

81
Q

Iv-dopamine

A
  • used in bradycardia + hypotension
82
Q

Adrenal enzymes
1 in first position: causes HTN
1 in second position: verulization

A

Enzymes: (+ hypokalemia with HTN only)

11–> HTN + Verulization
17–> HTN
21–> verulization

Internal Medicine Shelf Exam (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions