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Internal Medicine pt.1 > Pituitary > Flashcards

Pituitary Flashcards

1
Q

Where does the pituitary gland lie?

A

sella turcica

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2
Q

Where does the hypothalamus get its blood supply from?

A

superior hypophyseal artery -> internal carotid artery

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3
Q

Where does the pituitary gland get its blood supply from?

A
  • anterior lobe -> long portal veins from the hypothalamus

- posterior lobe -> inferior hypophyseal artery

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4
Q

What are the hormones secreted from the anterior pituitary gland?

A
  • Acidophils -> prolactin (TRH increases it & dopamine inhibits it) & Growth hormone
  • Basophils -> all the rest (TSH, ACTH, FSH, LH)
  • Chromophobes -> nothing
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5
Q

What are the hormones secreted from the posterior pituitary>

A

oxytocin & ADH

- synthesized in paraventricular & supraoptic nuclei of hypothalamus

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6
Q

What are the effects of pituitary tumors?

A
  • endocrine effects -> according to hormones
  • mass effects -> headache
    -> superior extension
    -> lateral extension: cranial 3, 4, 6 & ophthalmic division of 5 -> diplopia & facial pain
    temporal lobe dysfunction
    -> inferior extension: nasopharyngeal mass & CSF rhinorrhoea
    -> posterior extension: bilateral pyramidal tract signs
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7
Q

What is the effect of the superior extension of a pituitary tumor?

A
  • chiasmal syndrome -> decreased visual acuity & bitemporal hemianopia
  • hypothalamic syndrome -> SIADH (early due to irritation)
    - > disturbance of thirst, temp, appetite, & sleep regulation
    - > DI (late due to destruction)
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8
Q

When is a prolactinoma discovered?

A

in females -> micro adenoma

in males -> macro adenoma (doesn’t manifest until its larger)

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9
Q

What is the clinical picture of a prolactinoma?

A

1- compression symptoms
2- in females
- amenorrhea & galactorrhea
- hypoestrogen symptoms -> decreased libido & vaginal secretions, dyspareunia
-> osteoporosis
- hyperadrenergic symptoms -> hirsutism & acne
3- in males
- decreased libido & impotence
- oligospermia & infertility
- gynecomastia (rare)
4- delayed puberty

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10
Q

What are the investigations that should be done for prolactinomas?

A

basal prolactin levels

  • females -> 0-25ng/ml
  • males -> 0-20ng/ml

plain xray, CT, MRI
- to find tumor

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11
Q

How is a pituitary tumor treated medically?

A

Bromocriptine 2-5 times a day (dopaminergic agonist) - CABERGOLIN once a week (more effective)
- decreases hyperprolactinaemia
- restores menstruation, fertility, & stops galactorrhea
- decreases the size of the tumor
(continued for 1 - 2 years)

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12
Q

What are the side effects of bromocriptine?

A
  • short half life so taken 2-5 times a day
  • nausea
  • vomiting
  • postural hypotension
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13
Q

If medical treatment fails, what should be done next?

A

if tumor is <10mm (micro adenoma) -> trans-sphenoidal surgery
if tumor is >10mm (macro adenoma) -> trans-frontal surgery

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14
Q

What are the complications of a trans-sphenoidal surgery?

A
  • hypopituitarism
  • CSF rhinorrhea
  • meningitis
  • optic nerve damage
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15
Q

What is the inhibitory hormone of the growth hormone?

A

somatomedins (synthesized in the liver)

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16
Q

What regulates the growth hormone?

A

STIMULATION (GHRH)

  • hypoglycemia
  • stress, exercise
  • estrogen, clonidine, L-dopa

SUPPRESSION (somatomedins)

  • hyperglycemia
  • obesity
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17
Q

What are the effects GH hyper secretion?

A

acidophil pituitary adenoma
could lead to:
ACROMEGALY -> after fusion of epiphysis
GIGANTISM -> before fusion of epiphysis

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18
Q

What are the effects of gigantism?

A
  • massive growth of skeleton
  • soft tissue enlargement
  • early -> patient is strong
  • later -> weakness, hypogonadism, myopathy, peripheral neuropathy
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19
Q

What are the effects of acromegaly?

A
  • enlargement of acral parts (hands, nose, feet, jaw)

- progressive between the 2nd & 4th decades (manifestations appear 10 - 20 years later)

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20
Q

What are the facial & soft tissue features of acromegaly?

A

Facial

  • enlarged lips & nose
  • enlargement of mandible -> prognathism & increased spacing of lower teeth
  • macroglossia
  • enlargement of frontal sinuses
  • voice is cavernous & husky

Soft tissue

  • increase ring, glove, shoe & hat size
  • hands & feels are grossly enlarged (spade-like hands)
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21
Q

What are the neurological symptoms of acromegaly?

A
  • entrapment neuropathy -> carpal tunnel syndrome
  • peripheral neuropathy
  • proximal myopathy
  • mass manifestations
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22
Q

What are the cardiovascular & joint manifestations of acromegaly?

A
  • HTN
  • cardiomegaly
  • Raynaud phenomena
  • arrhythmias
  • sleep apnea
  • osteoarthritis of spine, knee, & hips -> late
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23
Q

What are the skin & metabolic manifestations of acromegaly?

A

SKIN

  • hypertrichosis
  • increased pigmentation -> acanthosis nigricans
  • warm, moist, & thickened

METABOLIC

  • secondary diabetes (glucose intolerance)
  • hyperhidrosis -> increased metabolic rate
  • hyperphosphatemia
  • hypercalcemia
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24
Q

What will be found on x-ray of acromegaly patient?

A

SKULL

  • thickening of cortex
  • pneumatisation of frontal sinus
  • prominent occipital protuberance
  • frognathism & big mastoid process
  • protrusion of the mandible

HANDS

  • mushroom appearance (pseudo clubbing)
  • brush border (tufting of terminal phalanges) -> periosteal thickening

HEEL -> thickening of heel pad >22mm

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25
Q

What will be found on ophthalmic exam of acromegaly patient?

A
  • bitemporal hemianopia
  • papilledema
  • optic atrophy
  • glaucoma -> if severe
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26
Q

What are the lab tests that should be preformed for diagnosis of acromegaly?

A

ENDOCRINAL

  • suppression test: failure of GH suppression in response to oral glucose load (to <2ng/ml)
  • IGF-1 levels increased (somatomedin)
  • GHRH increased from bronchial carcinoid (ectopic)

METABOLIC

  • increase BMR
  • hyperglycemia
  • hypercalcemia
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27
Q

What is the first line of treatment for acromegaly?

A

Surgical removal of acidophil pituitary tumor

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28
Q

When should medical treatment be done in cases of acromegaly?

A
  • when surgery is contraindicated
  • when in need for rapid relief of symptoms

Bromocriptine -> adjunctive therapy
Octreotide -> longer duration & more specific
-> side effect: vasoconstriction
Somatostatin -> very short half life & not specific for GH

29
Q

What are the causes of hypopituitarism?

A

1- infarction of the pituitary -> Sheehan, vasculitis, DM
2- infection & granuloma -> TB, syphilis, meningitis, sarcoidosis
3- idiopathic (congenital) -> deficiency of pituitary hormones
4- neoplastic -> adenoma, craniopharyngioma, leukemia, lymphoma, metastasis
5- physical agents -> radiation, surgery, trauma
6- miscellaneous -> haemochromotosis

30
Q

What is the most common cause of hypopituitarism?

A 
POSTPARTUM NECROSIS (SHEEHAN SYNDROME) 
- anterior pituitary most susceptible because its enlarged in pregnancy without increased blood supply
31
Q

What is the clinical picture of hypopituitarism in childhood?

A

PITUITARY DWARFISM (Levi-Laurain syndrome)

  • idiopathic decrease in GH
  • proportionate dwarfism
  • childish face
  • hypogonadism -> later

FROHLICH’S SYNDROME (dystrophia adiposgenetalis)

  • due to tumor or functional hypothalamus disturbance
  • dwarfism
  • hypogonadism
  • Samosa shaped obesity -> trunk & face only
  • Genu Valgum
  • hypothalamic disturbances -> DI, polyphagia, hypersomnia
LAURENCE-MOON-BIEDLE SYNDROME 
Fröhliches syndrome +
- mental retardation + skull deformity 
- retinitis pigmentosa
- polydactyly, syndactyly
32
Q

What is the clinical picture of hypopituitarism in adults?

A

1- panhypopituitarism - Simmonds disease

2- ISOLATED HORMONE DEFICIENCY

  • prolactin -> failure of lactation
  • GH -> silent
  • Gonadotropic hormones -> skin & sexual manifestations
  • ACTH -> hypoglycemia, inability to withstand physical & psychic stress, low resistance to infections, Addison’s or Simmond’s disease
  • TSH -> secondary hypothyroidism

3- general -> pressure manifestations
-> coma due to hypothermia, hypoglycemia, or pressure on brainstem or hypothalamus

33
Q

What are the manifestations of gonadotropic hormones?

A

Skin

  • fine & wrinkled
  • loss of secondary sexual hair progeria
Sexual manifestations 
Men 
- decreased libido 
- testicular atrophy 
- oligospermia

Women

  • vaginal dryness
  • dyspareunia
  • secondary amenorrhea
  • infertility
  • breast atrophy
34
Q

What is the difference between Addison’s disease & Simmond’s disease?

A

ADDISON’S primary hypoadrenalism

  • pigmentation due to stimulation of melanocytes
  • ACTH is increased
  • hypovolemia & hyperkalemia

SIMMOND’S secondary hypoadrenalism

  • absent pigmentation (lack of lipoprotein) + pallor
  • depigmentation of areola in females
  • ACTH & all other pituitary hormones are decreased
35
Q

How do we test for GH reserve?

A
  • measure GH level during sleep & then after exercise -> if level is > 6 then normal reserve
    if not > 6
    1- insulin induced hypoglycemia (0.1 U/kg IV)
    2- L-dopa
    3- Clonidine test
    samples are taken fasting & then at 60, 90mins -> if values are > 6 then normal
36
Q

How is LH & FSH reserve tested?

A 
normal gonadal function - to exclude hypothalamic or pituitary diseases 
- females -> normal menses 
- males -> normal sperm count 
if irregular 
1- measure basal LH & FSH 
if low 
2- LHRH (GnRH) test 
3- Clomiphene citrate test (estrogen antagonist) -> doubling the baseline LH & FSH
37
Q

How do we test for TSH reserve?

A
  • TRH test -> doubling the basal TSH level -> if low then secondary hypothyroidism
38
Q

How do we test the ACTH reserve?

A
  • insulin induced hypoglycemia -> increases cortisol level >10
39
Q

How is hypopituitarism treated?

A
  • Surgery in space occupying tumors
  • Radiotherapy if tumor is not entirely removed surgically or patient is unfit for surgery
  • Hormone replacement
    1- prednisone orally instead of ACTH (cortisol)
    2- L-thyroxine
    3- GH 3 injections BEFORE epiphyseal closure
    4- Testosterone or estrogen & progesterone if fertility is NOT needed
  • Human menopausal gonadotropin (HMG) or human chorionic gonadotropin (HCG) if fertility is needed
40
Q

what are the causes of pituitary apoplexy?

A
  • hemorrhage in pituitary gland
  • cerebrovascular accident
  • sickle cell anemia
41
Q

What is the clinical picture of pituitary apoplexy?

A
  • sudden headache (increase ICT)
  • meningeal irritation (pain)
  • sudden decrease in anterior pituitary hormones -> autohypophysectomy
  • Coma
42
Q

What investigations should be done for pituitary apoplexy & how should it be treated?

A

CT -> diagnostic -> hemorrhage will be seen
CSF -> bloody

1- surgical decompression
2- dexamethasone should be given (glucocorticoids)

43
Q

What are the general causes of short stature?

A

1- Primary defects -> in the skeletal system itself

2- Secondary defects -> systemic problems outside of the skeletal system

44
Q

What primary defects could lead to short stature?

A

1- skeletal dysplasia
2- chromosomal abnormalities -> Down & Turner syndromes
3- Inborn error of metabolism
4- genetic short stature -> pygmies

45
Q

What are the secondary defects that could lead to short stature?

A

1- intrauterine growth retardation -> infection, placental insufficiency, or maternal illness
2- idiopathic (most common)
3- malnutrition -> Kwashiorkor, marasmus
4- GIT diseases -> celiac, chronic liver, IBD, cystic fibrosis
5- renal diseases -> chronic parenchymal diseases, RTA
6- cardio-respiratory diseases -> Congenital heart diseases, asthma
7- endocrine diseases
8- psychological deprivation

46
Q

What are the endocrinal diseases that lead to secondary short stature?

A 
1- panhypopituitarism or isolated GH or GHRH insufficiency 
2- pseudohypoparathyroidism 
3- precocious puberty 
4- Cushing syndrome 
5- Cretinism
47
Q

How should short stature be assessed?

A

1- clinical features of disease
2- physical examination
- height to weight ratio
- specific physical findings for each disorder

48
Q

How can the height to weight ratio help us identify the diagnosis of short stature?

A

SHORT & UNDERWEIGHT

  • malnutrition
  • hypothyroidism
  • systemic diseases

SHORT & OVERWEIGHT

  • Cushing’s
  • decreased GH (decreases basal metabolic rate)
49
Q

What are physical findings of cretinism?

A
  • dry skin
  • coarse hair
  • depressed nasal bridge
  • big lips
  • protruding tongue
50
Q

What are physical findings of cushing’s syndrome?

A
  • central obesity
  • striae
  • HPN
51
Q

What are physical findings of Turner syndrome?

A
  • webbed neck

- coarctation of the aorta

52
Q

What are physical findings of pseudohypoparathyroidism?

A
  • moon face
  • obesity
  • short metacarpals
  • mental retardation
53
Q

How is short stature diagnosed & treated?

A

normal average height = father’s height + mother’s height/2 +- 6cm
if less than that then
1- treat the cause as early as possible
2- if idiopathic -> give GH BEFORE PUBERTY

54
Q

What are the effects of ADH (vasopressin) on the body?

A
  • increases absorption of water in the collecting tubules

- vasoconstriction

55
Q

What are the factors that increase ADH?

A

1- increased osmolarity
2- hypovolemia -> reflex stimulation due to decreased inhibitory impulses from the left atrium (less stretch)
3- hypotension -> baroreceptors are activated
4- higher centers stimulated by psychological factors & stress
5- pharmacological influence

56
Q

What are the pharmacological agents that increase ADH?

A 
1- acetylcholine 
2- beta-adrenergic agonists 
3- chlorpropamide 
4- carbamazepine 
5- cyclophosphamide 
6- nicotine & morphine

all lead to oliguria

57
Q

What are the pharmacological agents that decrease ADH?

A

1- diphenylhydantoin
2- naloxone

lead to polyuria

58
Q

What are the types of diabetes insipidus?

A
  • CENTRAL DI (pituitary or hypothalamus issue): low or absent ADH
  • NEPHROGENIC DI: kidney unresponsive to ADH

both cause polyuria of low osmolarity urine

59
Q

What are the causes of central DI?

A

1- FAMILIAL

  • dominant inheritance
  • recessive inheritance
  • DIDMOAD (Wolfram syndrome)

2- ACQUIRED any destruction of pituitary

  • trauma or tumors: in the brain
  • idiopathic (most common)
  • infections: meningitis, encephalitis
  • infiltrations: sarcoidosis
  • vascular: Sheehan syndrome
60
Q

What are the causes of nephrogenic DI?

A

ALL ACQUIRED
1- electrolyte disturbance
- hypokalemia -> primary aldosteronism
- hypercalcemia -> hyperparathyroidism

2- drugs -> lithium

3- diseases of the kidney

  • chronic renal failure
  • acute tubular necrosis (renal failure)

4- systemic disorders

  • amyloidosis
  • sickle cell anemia (causes shrinkage of kidneys)
61
Q

What is the clinical picture of DI?

A
  • polyuria -> polydipsia

- dehydration -> weakness, prostration, low grade fever

62
Q

What investigations are done to diagnose ADH insufficiency?

A

if patient is complaining of polyuria
1- exclude DM by glucose tests
2- urine analysis to confirm decreased ADH -> increase volume & decreased osmolarity
or stimulation tests
3- NaCl stimulation test
- normally -> increases osmolarity -> increases ADH -> oliguria
- if decrease in ADH -> no response
4- stimulation test by vasopressin (2-3 days IV)
- if still polyuria -> nephrogenic DI
- if oliguria -> either normal or central DI
or from the start
DEHYDRATION TEST

63
Q

How is the dehydration test preformed?

A

normally

  • dehydration -> increases ADH -> oliguria & increased osmolarity
  • give ADH -> less volume (oliguria) but osmolarity is the same

Central DI

  • dehydration -> no ADH -> polyuria & decreased osmolarity
  • when u give ADH -> oliguria & increased osmolarity

nephrogenic DI

  • dehydration -> increases ADH -> no response (polyuria & decreased osmolarity persist)
  • when u give ADH -> no response (polyuria & decreased osmolarity persist)
64
Q

How is central DI treated?

A

Hormonal replacement

  • vasopressin -> S.C
  • desmopressin (DDVAP) -> intranasal
  • vasopressin tannate in oil -> intramuscular

or

Non hormonal (drugs that increase ADH)

  • chlorpropamide
  • clofibrate
  • carbamazepine
65
Q

How is nephrogenic DI treated?

A

TREAT THE CAUSE
&
give hydrochlorothiazide (diuretic that decreases sodium) -> hyponatremia -> decreased water excretion

66
Q

What are the causes of SIADH?

A

increased ADH secretion & oliguria due to

  • malignancy: pituitary tumors or bronchogenic carcinoma
  • pneumonia, TB
  • cerebrovascular accidents
  • drugs: chlorpropamide, cyclophosphamide
  • hypothyroidism, ACUTE PSYCHOSIS
67
Q

What are the clinical findings in SIADH?

A
  • weight gain -> edema
  • lethargy, confusion, convulsion, coma: due to deceased osmolarity which leads to dilution hyponatremia + cerebral edema
  • oliguria
68
Q

What are the lab findings in SIADH?

A
  • decreased PLASMA osmolarity (<270)

- increased URINE osmolarity (>100)

69
Q

How is SIADH treated?

A

1- hypertonic saline infusion: increase in Na should not be more than 1-2ml/hr (to avoid cerebral dehydration)
2- restrict water intake
3- drugs that decrease ADH: diphenylhydantoin or naloxone
4- treat the cause

Internal Medicine pt.1 (33 decks)

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