Endocrine Diseases Flashcards
Adrenal Insufficiency causes :
- primary
- secondary and tertiary
- acute
- chronic
primary–addisons disease–MCC is autoimmune destruction of adrenal gland–>lack of cortisol and aldosterone
secondary–pituitary failure to secrete ACTH or suppression of HPA axis–>lack of androgens and cortisol
tertiary–hypothalamic disease and decr in CRH
acute–addisonians crisis
what happens if a PT is abruptly stopped on steroid tx?
adrenal insufficiency
- bc steroids provide exogenous negative feedback to the pituitary
- if steroids are stopped…the pituitary takes time to recover function–and during that time–adrenal insufficency can occur
in secondary adrenal insufficiency– ACTH is H/L and aldosterone is H/L??
ACTH–low
aldosterone–not affected so its normal
*of course low cortisol
MCC for acute adrenal insufficiency–Addisonians crisis
abrupt withdrawl of corticoid tx or a skipped dose of steroids
precipitating factors for addisonian crisis?
stressful event
- surgery
- illness
- trauma
- volume loss
- hypothermia
- MI
- fever
- hypoglycemia
- steroid withdrawl
MCC for addisonian crisis
abrupt withdrawl of glucocorticoids
imaging for chronic and acute adrenal insufficiency
CT: of the adrenal glands if unsure if insuff is autoimmune or not
CT imaging findings for Addison disease
small noncalcified adrenal glands
when do you see adrenal calcifications?
- tuberculous addison dz
- hemorrhage
- fungal infection
- pheochromocytoma
- melanoma
how to test for adrenal insufficiency (AI)
- order basic metabolic panel and do 8am measure of serum cortisol
- ->If results inconsistent with AI: consider other diagnosis
- ->If low cortisol levels, normal to high K and low to normal Na are found then go to: - Cosyntropin ACTH stimulation test: where we measure basal ACTH levels B4 administering IV ACTH–then we measure the cortisol levels after 30-60 mins
- –>if normal: consider other diagnosis
- –>LOW cortisol and HIGH acth–PRIMARY AI
- –>LOW cortisol and LOW acth–secondary AI - If primary AI:
- measure 21-hydroxylase antibody
- CT of adrenal glands
lab findings for primary adrenal insuff
- CRH
- ACTH
- cortisol
- Aldosterone
- Renin
- what would the ACTH stimulation test results show?
high CRH high ACTH low cortisol Low aldosterone high renin
ACTH stim tests would show: high ACTH
lab findings for secondary adrenal insuff
- CRH
- ACTH
- cortisol
- aldosterone
- Renin
- what would the ACTH stimulation test results show?
CRH: high ACTH: low Cortisol: low aldosterone: low Renin: normal to low
ACTH stim test: absent/low ACTH
lab findings for tertiary adrenal insuff
- CRH
- ACTH
- cortisol
- aldosterone
- Renin
- what would the ACTH stimulation test results show?
CRH: low ACTH: low Cortisol: low Aldosterone: low Renin: normal to low
ACTH stim test: exaggerated or prolonged
BMP results for adrenal insufficiency
- k
- na
- glucose
hyponatremia
hyperkalemia
hypoglycemia
list the disorders of HYPOfunction of adrenal glands
-both primary and secondary
PRIMARY
- ACUTE adrenal insufficiency–addisonian crisis
- addison’s disease
SECONDARY:
-pituitary failure of ACTH secretion–aka CHRONIC adrenocortical insufficiency
List the disorders of HYPERfunction of adrenal glands
-primary and secondary
- Cushing’s disease–SECONDARY
- Cushing’s syndrome
- Primary hyperaldosteronism
- Pheochromocytoma
Manifestations of ________ cause Cushing’s syndrome
Hypercortisolim
Hypercortisolism aka?
Cushing Syndrome
Different b/w Cuhsing’s DZ and Syndrome?
Disease: Pituitary Gland overprodues ACTH(due to hyperplasia or adenoma)—secondary cause of Hypercortisolim
Syndrome: s/s related to cortisol excess…..does not specify a cause of source of why excess cortisol.. has 4 main causes.. .ONE Of them is Cushing Disease
Four main causes of Cushing Syndrome
- Exogenous sources: long-term high dose glucocorticoids tx—-MCC overall!!!**
- Endogenous:
- over secretion of ACTh from AP—-cushing’s disease–MC endogenous cause!!!!!*******
* secondary
or
- Ectopic ACTH producing tumor/adenoma (MEN, SCLC)
- secondary
or
-Adrenal Tumor/adenoma (primary)
MC place for an ectopic tumor secreting ACTH
lungs—small cell lung Ca
low dose dexamethasone test is used as?
screening test for Cushing syndrome
when do we do high dose dexamethasone test??
after we get a negative result on low dose—- aka elevated cortisol levels
**used to distinguish a pituitary cause AKA cushing dz from an adrenal cause/other cause
Dexamethasone test results below indicate what cause of Cushing Syndrome:
- high ACTH with suppression of Cortisol
- High ACTH with no suppression of cortisol
- Low ACTH with no suppression of cortisol
- Cushing Dz (bc adrenals are sending neg feedback to AP—but AP is not listening)
- Ectopic ACTH producing tumor
- Adrenal tumor and/or exogenous steroids
list the three screening tests for cushing syndrome
*which is the most specific
- 24 hour urine test to test for cortisol-MOST SPECIFIC
- Nighttime salivary cortisol (11pm)
- Low dose 1 mg overnight dexamethasone test
if a low dose dexamethasone test does NOT suppress ACTH…..
indicates that cushing syndrome exists
but does not tell us the SOURCE of the increased cortisol—– why we do the high dose dex test
does an ectopic ACTH producing tumor respond to the negattive feedback?
NO
*why this test result will show as HIGH acth and no suppression of cortisol
When localizing the ACTH for dex test—- _____ responds to the negative feedback and _____ does not
Cushings disease DOES respond to neg feedback (why cortisol is supressed)
ECtopic ACTH prod tumor does not (why cortisol not supressed)
MCC of primary hyperaldosternoism
Bilateral adrenal hyperplasia
primary hyperaldosternoism is renin indep or dependen?
independent
Renin levels are NOT increased.. only seen with secondary
Conn syndrome is?
Adrenal Aldosternonoma—tumor in the zona glomerulosa secreting aldosterone
*primary form of hyperaldosteronism
triad for hyperaldosteronsm?
HTN— very very very drug resistant
HyPOkalemia
Metabolic alkalosis
PTs usually present how for hyperaldosteronism?
usually asympto
lab results for primary hyperaldosternoism?
HIGH aldosterone and normal renin 20:1 ratio -Hypok -hypernatremia high ph
labs for secondary hyperaldosternoism?
High aldosteron
high plasma renin levels—–because RAAS is activated due to renal artery stenosis– and increase in RAAS–increase renin–increase aldosterone
**NOT an adrenal issue here
define adenoma
a tumor that is non cancerous
Most common place for neuroendocrine tumors to arise?
why?
lungs and GI tract
WHY? because THEY LOVE BLOOD– love to grow in vascularized areas
**but since they are from neuroendocrine cells– they can arise technically anywhere
Characteristics of carcinoid tumors can cause?
carcinoid syndrome
carcinoid syndrome manifestations
flushing
diarrhea
wheezing
TSH secreting pituitary adenoma
- what is it
- size?
- invasive?
TSH producing adenoma… rare
- large
- very invasive
presentation for TSH secreting pituitary adenoma
diffuse goiter >95% of time
- hyperthyroid s/s
- pituitary adenoma s/s
lab work for tsh secreting pit adenoma
High TSH and High free T3/T4
- also can have some vision disturbances if its obstruction optic chiasm
- **because it is secondary hyperthyroidism
how to diagnose TSH secreting pituitary adenoma
MRI***
2. radioactive iodine uptake scan–will note diffuse uptake
radioactive iodine uptake scan–how does it work and for what hormone
TSH
-when TSH rises–thyroid gland uses iodine to make the T hormones–RAIU tests use a radioactive tracer (iodine) to measure how much tracer the thyroid gland absorbs
what disease will have diffuse uptake for RAIU
graves or TSH secreting pituitary adenoma
what disease will have decreased uptake for RAIU
thyroiditis
-hashimoto, postpartum
what disease will have “hot nodule or hot spot” uptake for RAIU
toxic adenoma
hot spot= focal area of increased uptake
what disease will have multiple nodules uptake for RAIU
toxic multinodular goiter
list the well differentiated thyroid CAs
papillary throid carcinoma
follicular thyroid Carcinoma
list the invasive and poorly differentiating thyoid CAs
Medullary thyroid carcinoma
anaplastic thyroid carcinoma
if she shows a pathology pic– which thyroid CA would it be?
papillary thyroid carcinoma
pathology shows “orphan Annie eye Nuclei”— what CA?
papillary thyroid carcinoma
which the MC thyroid CA?
papillary thyroid carcinoma
who have a poorer prognosis for papillary thyroid carcinoma.. men or women?
MEN**
who has a higher incidene rate for papillary thyroid CA?
WOMEN
which of the thyroid cancers is least aggressive and highest cure rate?
papillary thyroid carcinoma
which of the subtypes for DM1 is MC?
subtype 1A
when does 1A usually peak for onset?
young… ages 4-14
trigger for subtype 1A?
outside factors
- infection
- gene mutation: HLA DR3-DQ2 and DR4
MC clin man for DM1
hyperglycemia without acidosis
second MC clin man for DM1
DKA
normal body ph
- 35-7.45
* **7.40
DKA is MC seen with? and Hyperglycemic Hyperosmolar state MC seen with?
DKA–DM1
HHS–DM2
anion gap equation
+
normals for anion gap
[NA+] - [Cl-] - [HCO3]
normals range from 3-11 or 8-16
explain the presentation of diabetic neuropathy
stocking glove distribution–finger tips–fingers–hands—arms—–
or
toe tip–toes—foot–calfs—etc
*progresses distal–>proximal SYMMETRICALLY
what test is done to test for DM neuropathy
- monofilament test
- also can use the vibration sense test with tuning fork—if the PT cannot feel the vibrations from the fork… then move the fork proximally until they do feel it to sense their degree of neuropathy
target A1C to be below??
7
lab vlaues for DKA
pH <7.3 Bicarb <22 \+ketones in urine BGL >250... but usually not above 600 increased serum osmolarity
dawn phenomenon
- define
- describe patho behind it
- management
- normal glucose levels UNTIL
- ->2-8am
*results from decrease insulin sensitivity and nightly surge of counterregulatory hormones during nighttime fasting–>cortisol, glucagon, GH
- tx:
- bedtime injection of insulin (NPH) to blunt morning hypergycemia
- avoid nighttime snacks or CHO snacks late at night
Somogyi effect
- define
- describe patho behind it
- management
nocturnal hypoglycemia followed by rebound hyperglycemia
*due to surge in GH after the early AM hypoglycemia
tx:
- decrease nighttime insulin (NPH) dose
- give bedtime snack
- move evening dose of NPH to earlier
insulin waning
- define
- describe patho
- tx
progressive rise in glucose from bed–> morning
- seen when NPH evening dose is administered before dinner
- due to ineffective dosing of NPH insulin
tx:
-move NPH insulin dose to bedtime
or
-increase the evening dose
*happens a lot with newly diagnosed diabets who are unsure how todo nightttime dose
what is the main reason for delayed diagnosis of DM2
lack of overt s/s in the early disease process
**many PTs are diagnosed during anual screeings or incidentally with blood tests
ADA screening for DM
all adults greater than or equal to 45 X3 years
OR
BMI >25 in adults
explain patho behind poor wound healing in DM
DM patients have poor circulation bc their BVs are narrower–>glucose damages endothelium (constant inflammation)–>not enough oxygen is bound to hemoblogin–>less going to the area to be fixed
four diagnotic criteria for DM
- random glucose >200
- fasting glucose >126
- 2-hour postprandial glucose >200
- HgA1c>6.5%
differences b/w DM 1 and DM 2
- onset
- age of onset
- body habitus
- ketoacidosis
- Autoantibodies
- endogenous insuli
- concordance in ID twins
- Prevalence
DM1:
- onset=sudden
- age of onset=mostly under 30
- body habitus=thin or normal
- ketoacidosis=common
- autoantibodies=usually present
- endogenous insulin=low or absent
- twins=50%
- prevalence=less prev than DM2
DM2:
- gradual
- mostly adults
- often obese
- rare DKA
- absent antibodies
- insulin is normal decreased or increased
- 90% for twins
- more prevant—– 90-95% of US diabetics are type 2
is there a cure for DM1 or DM2?
NOPE
only maintenance
TOC for DM?
fasting plasma glucose levels
**check notes for the exact levels to diagnose preDM and DM
define impaired fasting glucose (IGF)
fasting glucose level of 100-125
define impaired glucose tolerance test (IGT)
plasma glucose levels 140-199 2 hours after a 75 gram glucose load
patients with IFG and IGT have DM?
no
-but are at very very high risk of developing DM2 and CVD in future
how to diagnose somogyi effect vs dawn? *what do we want to measure?
AM VMA (b/d of epinephrine) in the urine levels WHY??
because in somogyi—the hypoglycemia in middle of the night is a stressful event— so the body goes into FIGHT OR FLIHGT mode and secretes EPI, cortisol, glucagon etc….. compard to the dawn– no epi is releeasd
DKA is usually precipitated by?
recent infection
very commonly how do DM1 patients initially present?
in DKA
how often should DM patient get food exam
1-2 times per year
how often should DM get HBA1 checked
2-4 times/year by doctor
AND
DAILLLYYY by the PT
how often should DM get eye exam
annual or biannual
how often should DM get screening for neuropathy
annual
BP screening for DM done how often
quarterly
Which immunications is VERY imp for DM to get?
influzena
pneumococcal
Hep B
What is the MC cause of HHS and WHY
other precipitating factors
infection
*bc illness will lead to dehydration—->increased serum osmolarity–>leads to HHS
OTHEER:
- mi
- stroke
- surgery
what is the plasma glucose range in Pt with HHS
> 600
*DKA was lower like 250
plasma osmolarity for HHS?
> 320
what is not seen with HHS that is seen with DKA?
metabolic acidosis
HHS frequently occurs with?
mild or occult (“hidden”) DM
name meds that can cause HHS
phenytoin
diazoxide
corticosteroids
diuretics
typical pt population who gets HHS
middle-aged to eldery PTs
WHY? bc they are more prone to forget to take meds
onset of HHS?
insidious… usually over several days
clinical manifestations of HHS
weakness
polyuria
polydipsia
dehydration
AMS only when super advanced and serum osmolarity is over 310
convulsions occurs when serum osmolarity >320-330
PE findings for HHS
severe dehydration
lethargy
or coma (severe)
KUSSMUAL RESPS*****
general definition of pituitary adenomas
benign tumors that arise from one of the 5 AP cell types
*may cause clinical effects from either OVER prodcution of the hormone OR supression by compressive effects of structures
basically can cause:
-hypopituitaryism
or
-hyperpituitarism
**MC is over production
list the four cell types that pituitary adenomas can rise from
- somatotroph—->GH
- Lactotroph—>prolactin
- Corticotroph—> ACTH
- Thyrotrope—>TSH
which hormone secreting Pit tumor is MC?
prolactinomas—50%
what size of adenoma do you start seeing s/s?
2-10 cm
Lab values for prolactinoma
HIGH prolactin
LOW FSH and LH
**TSH, GH and ACTH levels are always ordered too bc prolactinomas can cause hyper or hyposecretion of these hormones
Lab values for Somatotroph adenoma
increase GH
about ____ of all pituitary adenomas are nonfucntions and do not secrete hormones
1/3
define microadenoma
<10mm
define macroadenoma
> 10mm
which pituitary adenomas are common to see in MEN1
prolactin and GH secreting tumors
general s/s for pituitary adenoma either hypo or hyper secreting
HA vision changes ---- bitemporal hemianopsia diplopia ptosis opthalmoplegia decreased facial sensation
can see hypopituitarism OR hormonal excess
MC cause of hyperprolactinemia
other causes
prolactinoma
primary HYPOthyroidism— because Increase TRH stimulates prolactin
aromegaly
pharmacologic: dopamine antagonists, 1st and 2nd gen antipsychotics, estrogen
physiologic:
- pregnancy
- stess
- exercise
s/s of hyperprolactinemia
- men
- women
- Men—hypogonadism (bc prolactin inhibits GnRH)
- Ed
- decr libido
- infertitlity - women–hypogonadism–oligomenorrhea, amenorrhea, infertility, vagina ddryness, galactorrhea
prolactin inhibits what hormone
GnRH
somatotroph adenoma causes?
acromegaly–>adults
gigantism–>kids
corticotroph adenoma causes?
cushing’s DISEASE
thyrotroph adenoma causes
hyperthyroidism
lab values for cortitotroph adenoma?
CUSHINGS DZ
so….
high cortisol
high acth
GH is a counterregulatory hormone that increases what?
glucose!
increase GH stimulates hepatic productino of?
IGF-1
*insulin like growth factor
lab values for gigantism/acromegaly
IGF-1 elevated (3-10 fold)
GH typically elevated–
which hormone do you use for diagnostic lab values to diagnose giantism/acromegaly
IGF-1 bceacuse it is more consistenly elevated compared to GH
complications from gigantism/acrpmegaly
LV diastolic HF cardiomegaly--cardiomyopathy glucose intolernce and DM colonic malignancy HTN
initial screening test of choice for gigantism/acromegaly
insluin-like growth factor lab values
what is the mortality rate for PT with giagantism
increases 3 fold compared to PT w.o
*survival rate 10 years less
confirmatory test for gigantism/acromegaly?
*results compared to pt w.o
oral glucose suppression test
-pt with disease will have elevated GH (bc normal response would be decreased)
image of choice for acromegaly or gigantism
MRI to check for pituitary lesions
high dose dexamethasone test results for cushings disease
cortisol will be suppressed
ACTH increased
TOC for cushings dz
MRI
dwarfism is?
GH deficiency–form of hypopituitarism
etiology for dwarfism
congenital or acquired
acquired—GH deficiecny from tumors, infiltrative diseases or pitutary infarction or radaition tx
- *pituitary does not make enough GH
- -can be in isolation or with generalized hypopituitarism
how to diagnose dwarfism
arginine and sleep stimulation test
Lab values for dwarfism
Low GH
Low IGF-1
arginine and GH
arginine stimulates GH
and inhibits somatostatin
arginine sleep study test–how does it work
if somene has dwarfism– what will results show
done after overnight fasting
samples are collected at the same time that GH would be peak stimulated
intervals when GH is measured: 0, 30, 60, 90, 120 minutes
MAX GH peak is around 60 minutes
+dwarfism will have no change in GH release
what is the diagnostic lab value to diagnose dwarfism
low serum IGF-1
osmolarity define
expressed as?
measured in?
changes with?
[ ] of solution
expressed as the total number of solute particles per liter
measured as milimoles/liters
changes with tempterature
define osmolality
measurd in??
affect with temp?
measure of the number of dissolves particles in a kg of the liquid they are dissolved in
*amt of dissolved substance (K NA CL Urea) in a sample of blood or fluid
measured in miliosmoles/kg
does not change with temperature
prefered in medicine
normal serum osmolality?
280-295 mOsm/kg
serum osmolality compared to osmolality inside cells
they are very close
what body fluid is used to measure osmolality in humans? and why
serum*****
urine too
it is very very very close to the osmolality inside the cells
define serum
what is left from blood once the cells and proteins have been removed
define serum osmolality
how much water is in the blood compared to how many solutes are in the blood
etiology for Central diabetes insipidus
NOOO production of ADH from PP
- **idiopathic MC
- head trauma
- not hereditary
- not genetic
- not autoimmune
what happens when there is no ADH production?
no reabsoprtion of water at the DCT back into the blood
- so volume regulation is out of whack
- body cannot concentrate urine–>large amounts of diluted urine–>increases serum osmolality
function of ADH
decrease urine production
decrease sweating
increase BP
*increases water absorption–>increasing intravascular volume–>dilutes serum sodium
clin man of DI
polyuria * like up to 20 times a day
polydipsia* excessssive thirst becayse body wants to maintian water balance with all the peeing
**high volume nocturia
Neuro s/s are from hypernatremia: confusion lethargy- disorientation seizures coma
PE findings for DI
dehydration
hypotension
rapid vascular collapse in severe cases
HYPOtensive
labs for central DI
increased serum osmolality >295 with inappropr diluted urine
decreased urine osmolality (<300) and Specific gravity +increased urine volume
HYPERnatremia
how to calculate serum osmolarity
(2x9Na+k) +(BUN/2.8) + (glucose/18)
definitive diagnosis of DI? what test
Fluid deprivation test: dont give the PT water….and a normal response is progressive urine [ ] (since the body is getting dehydrated)
BUT in DI:
they still produce large amounts of dilute urine with a low urine osmolality
how to differentite b/w DI central and nephorgenic? what test is don
Desmopressin ADH stimulation test
central= reduction in urine output + increase in urine osmolality (responding to ADH)
nephrogenic=contined production of large amts of diluted urine (No response to ADH)
define SIADH
causes what?
non-physiologic excess from ADH over secretion from AP
OR
from ectopic source
causes FREE WATER RETENTION AND HYPOnatremia—because retaining more and more water which is decreasing the sodium in plasma
*kidneys cannot excrete the excess water
what is the [ ] of urine for a pt with SIADH
very very concentrated
INCREASED urine osmolality
*urine sodium [ ] is very very high
etiologies for SIADH
MC?
MC: is CNS related–SAH, stroke, Head trauma, meningitis, CNS tumors, Post-op, hydrocephalus
Pulmonary causes: small cell lung CA** secreting ectopic ADH, infection (Legionella pneumonia), HIV
MEDS: Anticonvulsants, Carbamazepine, Hydrocholorothiazide, NSAIDS, chlorpropamide, antidepressants (TCAs/SSRIs), high dose IV Cyclophosphamide, MDMA, narcotics
OTHER: HIV, Conn syndrome and hypothyroidism
*mechanically ventilated patients are at risk for it too
Small cell lung CA.. always thikn of?
SIADH
**ectopic tumor producing ADH
Clinical Manifestations of SIADH
S/s vary depending on how rapidly the condition develops:
Nausea/Vomiting Neurologic s/s are due to hyPOnatremia & cerebral edema: -HA -weakness -lethargy -confusion -disorientation -Seizures ** -Coma
others:
* HTN
lab values for SIADH
Decreased serum osmolarity Decreased BUN decreased serum NA+ ***in the setting of normovolemia aka no s/s of edema HIGH ADH Increased Urine somolarity with NA+ >20
**diagnosis made in absence of renal, adrenal, pituitary, thyroid diseases or diuretic usage
differences b/w Cenrtral DI and SIADH
- ADH and water
- urine output
- sodium
- serum osmolairty
- Risk of developing___?
- Tx
for Central DI:
- low ADH and low water in body
- very high UO +polyuria
- serum NA high–hypernatremia
- high serum osmolalty due to dehydration
- risk to develop hypovolemic shock
- DDAVP –synthetic ADH
SIADH:
- high ADH and high water in body
- decreased UP—Oliguira
- low soidum–hyponatremia
- low serum osmolarity
- risk of developing seizures from hyponatremia
- Hypertonic Saline
oliguria
little urine prod
CDI and SIADH pneumonics
SIADH—- Soaked Inside
DI—Dry Inside
etiologies for hypocalcemia
MC?
MCC hypoparathyroidism ***
chronic renal disease or liver disease
Vit D deficiency–osteomalacia and rickets
Hypomagnesia
MEDS: diruetics, Ca chelators, bisphosphonates, denosumab
hypocalcemia occurs at a level below____ mg/dl
8.0
functions of CAclicum
blood coagulation
neuromusc actiivty
cellular acitivty
bone integrity
most of CA is bound or unbound?
BOUND to albumin **why we get “corrected” levels*
Calcium levels are controlled by?
PTH–increaeses levels
Calcitonin–decreases levels
Vit D–increases levels
if calcium is low and PTH is high… explain some etiologies behind this
- VIt D deficiency is causing hypocalcemia—the parathyroid is releasing PTH in response
- PTH itself may be abnormal/non functional
- PTH receptors may be resistant to PTH–leading to elevated serum PTH and ineffective hormone–also called pseudohypoparathyroidism
pseudohypoparathyroidism
when PTH receptors are resistant to PTH–leading to increases levels of PTH and hypocalcemia
*caused by G protein and malfunction of the signal transduction inside the cell
s/s of hypocalcemia
most are asympto
CNS: fatigue, irritability, depression, anxiety, congnitive impairmnt, lethargy, paraesthesias–hands/feet also at circumoral area, also parkinsonian s/s due to brain calcification
MSK: increased muscular contractions—bc hypocal decreased excitation threshold–increased muscle and nerve excitability—>MUSCLE CRAMPS, convulsions, BRONCHOSPASMS with stridor, FINGER PARESTHESIAS, carpopedal spasms, Chvostek sign, increased DTR
Arrythmias
dry skin, psoriasis
Diarrhea, abd pain, or cramps
abnormal dentintion, osteomalacia
cataracts
ECG findings for hypocalcemia?
prolonged QT
two main PE findings for hypocalcemia/hypoparathyroidism
- Chvostek sign: facial muscle contraction/spasm occuring when you tap on the facial nerve
- trousseau’s sign: carpal spasm with inflation of a BP cuff above the SBP
CATS-G
s/s for hypocalcemia
convulsions arrhytmias: prolonged QT--torsades, CHF tetany and DTR increased spasms and stridor GI--N/V/ constipation,
Etiologies for hypoparathyroidism ? MC?
RARE
Primary MC: autoimmune destruction of the parathyroid glands
issues with parathyroid synthesis
Seconary MC: post thyroidectomy surgery via accidental removal of parathyroid gland OR parathyroidectomy—–accquired
**surgical reason is more common than the auto immune destruction
OTHERS:
- hypo or hypermagneisum–REVERSIBLE
- radiation therapy
- congential pseudohypoparathyroidsm, parathyroid hypoplasia (DiGeorge Syndrome)
clinical manifestations of hypoparathyroidism
RELATED TO HYPOCALCEMIA:
- CNS: fatigue, irritability, depression, anxiety, cognitive impairment, lethargy, paraesthesias @circumoral area and hands +feet, seizures, increased DTR
- MSK: weakness, cramps, carpaldpedal spasms, convulsions, tetany, laryngospasms and stridor
- Cardio: prolonged QT—torasdes
- Skin: dry, skin psoriasis
- GI: diarrhea, cramping/abd pain,
long term hypocalcemia with hyperphosphatemia causes ?
calciications in the soft tissues like joints skin artieries
brain calcifications in BG
PE findings for hypoparathyroidism
Chvostek sign
Trousseuas sign
EKG can show prolonged QT
labs for hypoparathyroidsm
TRIAD:
decreasd intact PTH
hypocalcemia
increased phosphate
urine studies:
- ca low
- alkaline phosphate normal
always measure serum mag too beacuse hypo or hyper mag can exacerbate symptoms
hypocalemia + HIGH PTH can be from?
renal or liver diz **
vit d deficinecy
hypomagnesium
hypocalcemia + low PTH etiology?
hypoparathyroidism MC
etiologies for hyperparathyroidism
PRIMARY:
- parathyroid adenoma–screting PTH— MC cause
- Lithium
- MEN 1 and MEN 2A (rare)
SECONDARY:
-incr PTH by physiologic response to hypocalcemia or vit D deficiency—CHRONIC KIDNEY DZ MC ***
CM of primary hyperparathyroidism
most asymptomatic
But, get s/s of hypercalcemia
STONES: kidney stones from renal loss of CA and phosphate, NEPHROLITHIASIS–ca oxalate and phosphate deposition
BONES: increasd osteoclastic activity causing:
- decalcification of bone –PAIN
- easily fractured
- pseudotumors in the jaw, skul, and phalanges
- osteopenia
- osteoporosis
- decreased DTR
ABD GROANS: incr CA stimulates gastrin release–causeing ulcers
- abd pain
- acute pancreatitis
- increase gallstones
- constipation
- N/V
PSYCHCI MOANS:
- depression
- anxiety
- behaviroal changes
HTN
lab values for primary hyperparathyroidism
both blood work and urine studies
TRIAD: for blood work
HIGH Calcium
high intact PTH
LOW phosphate
urine:
- hyperphosphaturia
- hypercalciruria
Lab values for secondary hyperparathyroidism
normal-low CA
high phosph
high PTH
super low Vit D
diagnostic tests for hyperparathyroidism
labs
bone density scan– will show osteoporosis
Ultrasound to see if PTH adenomas
how does high PTH raise blood ca?
- breaking down the bone– taking our the CA from bone
- increasing body’s ability to absorb CA from GI tract
- increasing kidneys ability to HOLD onto CA that otherwise wouldve been lost in urine
increase serum and urine CA*
EKG findings for hypercalcemia?
shorteend QT interval **
Prlonged PR
QRS widening
lab values for CA and PTH in the following:
- hyperparathyrodism
- hypoparathyroidism
- hypercalcemia of malignancy
- secondary hyperparathyroidism in renal dz
- high for both
- low for both
- high CA and low PTH
- low CA and high PTH
