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Internal medicine 1 > internal medicine 1 endocrinology > Flashcards

internal medicine 1 endocrinology Flashcards

1
Q

causes hypopituitarism?

A
  1. congenital: prader willi (del15) –> hypogonadism + Kallman syndrome (no neural migrations thus no GnRH –>no LH nor FSH –> hypogonadism + Empty sella syndrome
  2. aquired
    - trauma, surgery, radiation damaging pituitary gland
    - tumors: adenoma or metastasis
    - infection: toxoplasma
    - Sheenhan post partum necrosis (no bloodsupply thus necrosis of pituitary) –> no postpartum lactation, loss of pubic hair
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2
Q

hormones of anterior pituitary?

A

GH, FSH/LH, ACTH, TSH, PRL

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3
Q

hormones of posterior pituitary (neurohypophysis)?

A

ADH, oxytocin

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4
Q

examples of hyperfunctions of anterior pituitary?

A
  • Prolactinoma –> galactorrhea, amenorrhea, infertility, bipolar hemianopsia
  • cushings disease
  • acromegaly (adult) giantism (kids)
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5
Q

diabetes insipidus 2 types?

A
  1. central type: ADH deficiency due to eg. post.pituitary tumor
  2. nephrogenic type (more common): no ADH receptors in kidney
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6
Q

symptoms of diabetes insipidus?

A

polyuria, polydipsia (crave cold water)

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7
Q

dx of diabetes insipidus?

A

Water deprivation test:
aim: differentiate from psychogenic polydipsia
measure urine density –> no water for 8 h –> measure urine density again, positive if low urine density
psycogenic if high urine density

desmopressin test (ADH analog)

aim: differentiate nephrogenic from central
central: respond to test by increase H2O absorption from kidney
nephrogenic: no respons to test (bc. no ADH receptors doesnt matter if we give ADH)

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8
Q

SIADH meaning?

A

syndrome of inappropriate anti-diuretic hormone:

high levels of ADH in blood

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9
Q

causes, symptoms, tx of SIADH

A

causes examples: ADH producing small cell lung carcinoma, opioids, stroke

symptoms: low urine output, increased serum hypoosmolarity, hyponatremia –> nausea, vomit
tx: dont drink so much water, demeclocycline

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10
Q

causes of hypothyroidism?

A
  1. primary hypothyroidsm
    - Hashimotos autoimmune thyroiditis #1
    - surgical removal, viral infection, congenital
  2. secondary hypothyroidism
    - damaged ant. pituitary (no TRH no TSH)
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11
Q

symptoms of hypothyroidism?

A

decresed BMR thus weight gain, fatigue, intolerance to cold, goiter/struma, muscle ache and weakness, bradycardia, myxedema (accumulations of glycosaminoglycans in skin and soft tissue –> deepening of voice and large toung)

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12
Q

3 stages of Hashimoto?

A
  1. initially hyperthyroidism due to ANTI-TG-AB causing damage of thyroid follicles thus release of thyroid hormones.
  2. symptoms of euthyroid when decrease of hormone cc
  3. final hypothyroidism
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13
Q

dx of hypothyroidism?

A

elevated TSH, clinical symptoms, autoabs
ANTI-TG-AB (thyroglobulin)
ANTI-TPO-AB (thyroid peroxidase)

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14
Q

hypothyroidism and infertility connection?

A

50% of patients with hypothyroidism have prolactinemia bc. TRH increase TSH and PRL
PRL cause failure to sustain the fertilized egg thus loss of early pregnancy (infertility)

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15
Q

hyperthyroidism causes?

A
  1. Graves #1 (autoimmune- ANTI-TSHreceptor-AB) TRAB
  2. Destructive thyroiditis aka De Quervain (post viral infection)
  3. Toxic (hormone producing) adenoma
  4. Thyroid hormone overdose
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16
Q

symptoms of hyperthyroidism?

A

increased BMR thus weight loss, exophthalmos (bulging of eyes due to retrobulbar CT edema)–> swelling of extraocular muscles –> compress optic n. –> vision loss, struma/goiter (in both hypo and hyper)

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17
Q

3 categories of thyroiditis?

A

acute, subacute, chronic

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18
Q

example of acute thyroiditis?

A

Acute infectious thyroiditis due to eg. E.coli, severe neck pain radiating to ear

(non-infectious due to eg. radiotherapy as side effect due to thyroid malignancy)

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19
Q

example of subacute thyroiditis?

A

De Guervains (subacute granulomatous thyroiditis)
post viralinfection eg. adenovirus “cold” causing granuloma formation in thyroid
sym: painful dysphagia, fever neckpain after URT infection
-initially hyperthyroidism when gland is damaged by granuloma reaction and thus hormones released into blood, few (15%) become hypothyroid after inflammation decrease.

Note: importance to diff. from Graves since this form of hyperthyroidism is self-limited 6 w (vs. Graves: radioiodine tx)

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20
Q

example of chronic thyroiditis?

A

Hashimotos autoimmune thyroiditis
-ANTI-TPO-AB
-ANTI-TG-AB
destruction of thyroid gland, inflammatory infiltrade, CD8+ cells kill thyroid cells, B cells produces the ABs

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21
Q

Goiter=struma meaning?

A

painless thyroid enlargement

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22
Q

thyroid malignancies?

A
  1. follicular adenoma
  2. papillary carcinoma #1
  3. follicular carcinoma
  4. anaplastic carcinoma
  5. thyroid medullary carcinoma (c-cells)
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23
Q

follicular adenoma characteristics?

A

solitary, non-funtional thus “cold nodule” with nuclear medicine

  • may progress to carcinoma
  • if TSH R. mutation –> increase thyroid hormones –> functional toxic adenoma “hot nodule” (rarley become malignant)
    dx. UL
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24
Q

papillary carinoma characteristics?

A

1

  • any age, non functional
  • MAP kinase pathway overactivated
  • painless neckmass
  • 50% metastasize to cervical LN + lung + bone
  • prognosis: 90% survive 10 yrs
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25
Q

follicular carcinoma characteristics?

A
  • women 50+
  • painless neckmass
  • NO cervical LN metastasis (how to differ from papillary carcinoma) spread to blood.
  • invasive of thyroid capsule (how to differ from follicular adenoma)
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26
Q

anaplastic carcinoma characteristics?

A
  • oldies 65+
  • very agressive, almost 100% mortality, death in 1 year
  • p53 mutation
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27
Q

thyroid medullary carcinoma characteristics?

A
  • origin from parafollicular C cells (of medulla that make calcitonin that decrease calcium by inc. renal extretion)
  • MEN2 (RET oncogen) 30% but mainly sporadic 70%
  • prognosis: median survival 5 yrs (aggressive with quickly metastasis)
  • no hypocalcemia even if increased calcitonin (tumor marker) bc. the tissue get resistant to calcitonin
    symptoms: painless neckmass, compressionsymptoms:hoarsness,dyspnea,dysphagia,cough
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28
Q

Cushing´s syndrome def?

A

glucocorticoid excess in the blood (exogenous or endogenous) that causes a group of symptoms

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29
Q

symptoms cushings syndrom?

A
  • moon face
  • central obesity (fat belly skinny legs)
  • red stria on abdomen
  • buffalo hump = fat deposit on back of neck
  • hyperpigmentation (incr. ACTH –> incr. alpha-MSH –> hyperpigm.)
  • HTN (if too high glucocorticoid cc they also stimulate aldosterone receptor –> H2O retention –> incr. BP)
  • incr. glucose –> DM
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30
Q

cushings disease

A

cause cushings syndrome due to:

ACTH producing pituitary adenoma or hypothalamic CRH secretion –> inr. ACTH

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31
Q

dx and differentiation of cushings syndrome and disease?

A 
Dextrametasone test (cortisol analogue)
- LOW dose administration:
cortisol is suppressed --> Cushings syndrome

-HIGH dose administration:
ACTH is suppressed by negative feedback thus cortisol decr. in blood –> Cushings disease
(ectopic ACTH producing adenomas cannot be suppressed)

other test of cushings syndrome:

  • 24 h urine cortisol level will be increased
  • late night salivary cortisol level will be increased
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32
Q

Primary hyperaldosteronism AKA CONN’s SYNDROME ?

A

high aldosterone level and LOW renin
triad symptoms: HTN, hypokalemia, HYPERnatremia + metabolic alkalosis

cause:
- aldosterone producing adenoma (unilateral)
- bilateral adrenal hyperplasia
- carcinoma rare

tx:

  • if adenoma/carcinoma: surgical removal
  • hyperplasia: sporonolactone (aldosterone receptor antagonist)
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33
Q

Pheochromocytoma?

A
  • benign neuroendocrine tumor of adrenal medulla
  • origin from chromaffin cells (E and NE producers)
  • overproduction of E and NE (catecholamines) cause symptoms triad: sweating, headache, tachycardia
    other symptoms: HTN, palpitation, nausea
    10% rule: extraadrenal, bilateral, not associated with HTN, biologically malignant.

dx. chromogranin A neuroendocrine tumor marker
high cc VMA catecholamines metabolites
CT

tx. removal adrenal gland, supress NEandE producaiton

34
Q

Addisons disease?

A

aka chronic adrenal insufficiancy

more 90% of adrenal cortex non funtion thus neither cortisol or aldosterone

35
Q

addisons cause?

A 
#1: autoimmunity destruction of adrenal cortex 
others: TBC, metastatic carcinoma from lung
36
Q

symptoms, dx, tx of addisons disease?

A

symptoms: weakness, hyperpigmentation, hypotension
dx: ACTH stimulation test (result: no cortisol)
tx: steroid replacement for life (cortisol and aldosterone)

37
Q

Primary amenorrhea definition and cause?

A

def: no menstrual period by age 16
cause: #1 gonodal development failure

38
Q

Secondary amenorrhea definition and cause?

A

def: abscence of menstrual period for 3 cycles or more than 6 month in a woman who had menses

cause:
- chronic anovulation
- Anorexia (BMI less than 17)
- hyperprolactinemia (prl inhibit GnRH thus no LH nor FSH –> amenorrhea, infertility)
- Polycystic ovarian syndrome

39
Q

Male hypogonadism?

A

1 Kleinefelter syndrome XXY trisomy

def: failure of testosterone production

  • impaired Testosterone production by leydig cells –> primary hypogonadism (infertility)
  • underdiagnosed detected in adulthood when they cannot have children
    tx: lifelong testosterone

other causes of hypogonadism:

  • Prader willi (del15)
  • Kallman syndrome (no nerual migration thus no GnRH thus nu FSH nor LH)
40
Q

Hirtuism meaning?

A

male like hairgrowth in women eg. beard, chest hair

41
Q

Virilization meaning?

A

excessive sex hair growth + overallt increased hair growht

  • less frequent than hirtuism
  • reflect severe underlying condition eg. male hormone producing tumor
42
Q

differential diagnosis of hirtuism?

A
  • Cushings syndrome
  • PCOS (polycystic ovarian syndrome)
  • Virilization
  • Anabolic drungs
43
Q

testosterone function?

A

bind androgen receptors causing:

  • increased hair follicle size
  • increased sebum secretion –> acne
44
Q

PCOS (polycystic ovarian syndrome) characteristics?

A 
symptoms: hirtuism, obese, subinfertility
#1 cause of hirtuism

The exact cause of PCOS isn’t known. Factors that might play a role include:

  • Excess insulin. Insulin is the hormone produced in the pancreas that allows cells to use sugar, your body’s primary energy supply. If your cells become resistant to the action of insulin, then your blood sugar levels can rise and your body might produce more insulin. Excess insulin might increase androgen production, causing difficulty with ovulation.
  • Low-grade inflammation. This term is used to describe white blood cells’ production of substances to fight infection. Research has shown that women with PCOS have a type of low-grade inflammation that stimulates polycystic ovaries to produce androgens, which can lead to heart and blood vessel problems.
  • Heredity. Research suggests that certain genes might be linked to PCOS.
  • Excess androgen. The ovaries produce abnormally high levels of androgen, resulting in hirsutism and acne
45
Q

hypercalcemia def?

A

more than 2.6 mM EC Ca2+

normal: 2.2-2.6 mM
- 15% of hostpitalised patients
- medical emergency

46
Q

hypercalcemia symptoms?

A 
CNS: depression, coma
GI: vomit, nausea
Muscles: weakness
HTN, bradycardia, short QT inverval
kidney stones
metastatic calcifications
bone pain fracture
47
Q

differential diagnosis/cause hypercalcemia?

A
  • # 1 primary hyperparathyroidism
  • ectopic PTH producing tumor eg. small cell lung cancer
  • bone destruction disease eg. multiple myeloma/metastasis of bone
  • excessive Vit D intake (vit D needed to absorb Ca2+ from GIT)
  • renal insufficiency (cannot be excreted via urine)
48
Q

tx hypercalcemia?

A
  • dont eat things with it
  • stimulate kidney ca2+ secretion
  • inhibit bone reabsorbtion
  • treat underlying condition
49
Q

hypocalcemia def?

A

less than 2.2 mM serum ca2+

50
Q

differential diagnosis/causes of hypocalcemia?

A
  • hypoparathyroidism dye to eg. removal of thyroid, irradiation, DiGeorge
  • chronic kidney disease
  • vit D deficiency due to eg. malabsorption
51
Q

symptoms of hypocalcemia?

A

muscles: tetany, spasm
CNS: irritability
HF, longer QT interval

52
Q

signs of hypocalcemia?

A
  1. Chovostek’s sign: twitching of facial muscles in respons to tapp on area in face where facial n. is
  2. Trousseau’s sign: hand flex when inflating the blood pressure cuff to a level above systolic pressure for 3 min
53
Q

Osteoporosis 4 main features?

A
  1. General disease thus whole skeleton involved
  2. Progressive disease thus a continous decrease in bone mass
  3. Detoriation in bone microstruction
  4. increased bone fragility increasing risk of low trauma fracture
54
Q

dx osteoporosis?

A

DEXA Tscore more than -2.5 SD + clinical symptoms
NORMAL ca2+ , phostphate, PTH cc

note that other causes can have decreased Tscore eg hyperparathyroidism - 3 SD..

55
Q

tx osteoporosis?

A

Bisphosphonate (induce apoptosis of osteoclasts)

56
Q

Osteomalacia(adults) Rakit (children) characteristics?

A

def: vitamin D deficiency resulting in decreased bone mineralization thus less strenght
symptoms: fractures, deformed bone, forward sternum “pigeon breast”

57
Q

History of osteomalacia/rakit –> “English disease”

A

during industrialization in england people moved from sunny contryside into the dark cities, less sun less vit D
–> less ca2+ and P04+
after a while children got coxa vara & valga (ko och hjulbent)

58
Q

MEN def?

A

MEN = multiple endocrine neoplasia

  • group of inherited diseases causing proliferative lesions of endocrine organs
  • MEN 1 & 2 most common
  • arise usually in youg age
59
Q

MEN-1?

A
  • MEN-1 gene is a tumor suppressor gene on chr. 11
  • inactive MEN-1 gene –> uncontrolled cell proliferation
  • organ involvement “3 P’s”
    1. Parathyroid –> hyperplasia –> #1 primary hyperparathyroidism
    2. Pancreas eg. inulinoma
    3. Pituitary eg. PRL secreting macroadenoma
60
Q

MEN-2A & MEN-2B?

A

-MEN-2 (RET oncogen) on chr. 10

MEN2A:

  • thyroid medullary carcinoma (parafollicular c-cells)
  • phenochromocytoma (chromaffin cells)
  • parathyroid hyperplasia –> primary hyperparathyroidism)

MEN2B:

  • thyroid medullary carcinoma
  • phenochromocytoma
61
Q

thyroid medullary carcinoma and RET mutation?

A

check rest of family becouse very aggressive cancer that can be prevented by thyroid removal

62
Q

classification of DM?

A
  • type 1 DM: insulin deficiency due to auto-B-ab destroying insulin islets
  • type 2 DM: insulin resistancy due to eg. IRS phosphorylation caused by obesity

other:
-MODY (maturity onset diabetes of young)
monogenic type
- “Bronze diabetes”
due to hematochromatosis, iron accumulate in skin causing increased melanin production hence name + destruction of pancreas
- gestational diabetes (obesity risk, usually go away after pregnancy)
- LADA (latent autoimmune diabetes of adults)
new name: slowly evolving immune mediate diabetes in adults = mild type of DM with progressive destruction of B cells due to autoimmunity, take years

63
Q

Dx of DM?

A
  1. clinical symptoms: polyuria, polydipsia
  2. urine test: presence of glucose or KB
  3. blood test:
    -fasting glucose more than 7 mM
    - anytime glucose more than 11 mM
  4. Auto ABs if DM1
  5. glycosylated hemoglobin (HbA1c)
    more than 6.5% increases risk of DM complications (higher worse)
  6. C-peptid not good for dx. since long half life in blood

note: DM2 usually detected by chance eg at opthalmologist

64
Q

triad of DM tx?

A

Diet, exercice, medication (orals and insulin)

65
Q

tx DM –> DIET?

A

160 g carbs/day
1/3 carbs, meat, salad
dont eat after 18 pm

66
Q

tx DM –> ORAL antidiabetic agents?

A
  1. # 1 Metformin: increase insulin sensitivity.dont take 2 days before CT with contrast agent or else kidney damage
    side effects: diarrhea, abdominal distension (to avoid start with low dose and increase gradually)
  2. GLP-1 analog (incretin)
  3. SGLT-2 inhibitor (kidney glucose transporter)
67
Q

Incretin effect?

A

show the importance of incretins.

upon eating incretins are secreted by GIT to induce insulin secretion thus if you give parenteral glucose you dont take advantage of this effect.

68
Q

tx DM –> Insulin and insulin analogues?

A
  • human classic insulin (cheaper+peak) vs insulin analougues (less hypoglycemic risk bc. no peak more steady)
  • rapid acting vs long acting

Insulin administration:

  • subcutaneous
  • pumps
  • inhaled

note: important to know tx if you wanna change u dont wanna cause hypoglycemia

69
Q

complications of DM?

A
  1. Microvascular complications:
    - retinopathy –> blindness
    - nephropathy –> proteinuria (kidney damage)
    - neuropathy –> diabetic foot
  2. Macrovascular complications:
    - stoke
    - AMI
    - HTN
neuropathic leg
warm/normal and normal skin color 
worse pain during night
"glove and sock" pain distribution
(vs. atherosclerotic pale/purple and cold)
70
Q

hyperglycemic emergencies?

A
  1. Diabetic ketoacidosis (DKA)

2. Hyperosmolar hyperglycemic state (HHS)

71
Q

Diabetic ketoacidosis?

A 
#1 cause of death in children and adolecence with DM-1
sym: nausea due to acidosis thus vomit to remove excess acids, hyperventilation (Kaussmaul's breathing) with ketone smell, coma

Lab/Dx: low pH, incr. blood and urine glucose, hyperkalcemia

Tx: 0.9% saline solution for dehydration + insulin

72
Q

Hyperosmolar hyperglycemic state?

A
  • usually in DM2 patients
    sym: tired bc. dehydrated due to excessive glucose causing osmotic diureses, coma

tx: like Diabetic ketoacidosis with saline and insulin but usually more saline solution needed to hydrate patient.

73
Q

Hypoglycemia?

A

sym: seizures, tachycardia, cramps, coma

cause:
if DM: too much insulin, heavy workout, bad food/insulin balance
if not DM: insulinoma, alcohol overconsumption
others:fever, sepsis (some bacteria eat glucose), addisons, liver disease (no GNG)

tx. glucose

74
Q

Whipples triad: sign of hypoglycemia?

A
  1. less than 3 mM glucose
  2. relief in symptoms after eating glucose
  3. CNS symptoms (caused by less than 3 mM)
    c-confusion
    n-nervousness
    s-syncope
75
Q

Disorders of lipoprotein metabolism? examples

A

Familial hypercholesterolemia #1

  • AD, 1/500, LDL receptor mutation
  • Homozygous(both LDLreceptor alleles mutated): 30% die from AMI before 30 yrs
  • Heterozygous: 50% risk of CAD before 50 yrs
  • sym: atherosclerotic plaque, xanthoma (lipidaccumulation under skin, yellow papule on buttucks, knee,hands)

others:
ApoB mutation 1/1000
ApoE mutation 1/10000

76
Q

Gout def?

A

def: uric acid accumulation due to overproduction or underexcretion or both.

uric acid is the final product of purine degredation extreted by the kidney, if excessive form crystals in joints causing inflammation “crystal arthritis” –> swollen and painful joints

77
Q

dx and tx of Gout?

A

Dx: clinical symptoms/history + joint aspiration –> polarized light microscope show crystals
HIGH SERUM URIC ACID DOES NOT MEAN THAT THE PATIENT HAS GOUT

Tx: treat acute symptoms and prevent progress

  • acute treatment: NSAID, corticosteroids, Canakinumab (anti-IL-11-ab)
  • prophylaxis: life style(less meat and alcohol), drug therapy Allopurinol (xanthine oxidase inhibitor)
78
Q

Untreated Gout complication?

A

Chronic Tophaceous Gout

  • more joints involved
  • formation of “Tophi” = crystals in soft tissues
  • X-ray sign: Bone erosions of joint surface
79
Q

symptoms of intoxications?

A
  • CNS:seizure, coma
  • Vomit, nausea
  • sudden onset of unexplained illness
80
Q

General management of intoxication?

A
  1. support ABC (airway, breathing, circulation)
  2. try to figure out what poison (BUT treat patient, not poison)
  3. maintain body T
  4. rule out other cause eg. neurological, metabolic disease
  5. remove poidon from boby by lavage (wash out stomach/colon) “magpumpa”
  6. Inhibition of absorbtion: Activated charcoal (form protective layer in stomach thus less poison absorbed) DONT GIVE IF METHANOL, CYANIDE,TYLENOL
81
Q

poison and antidote?

A

poison (methanol) antidote (ethanol)

opioides — naloxone

82
Q

pin-point pupils?

A

pin-point pupils sign of eg. morphine (opiate) bc. enhance parasympatetic system vs. cocaine dilation via sympatetic activation

Internal medicine 1 (1 decks)

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