Endocrine Disorders Flashcards
Overview of the Endocrine System
- Endocrine gland secretes hormone into bloodstream where it binds to either (2)
-
Active hormone = ______, able to bind to its receptor
- Some hormones are activated by _____ or other periphral tissue, so being ______ by kidney or liver activates them
- (1): its receptors are located on the plasma membrane and operates through second messenger system to create physiological response
- (1): receptors on plasma membrane, cytoplasm receptor, or nuclear receptor
- Whatever the physiological response is = source of ______ regulation to the secreting gland
- albumin or hormone specific binding protein (testosterone, estrogen, progesterone)
-
Unbound
- liver, metabolized
- Water soluble hormones
- Lipid soluble hormones
- Feedback regulation
Arrows in this Diagram
Represents potential source of alteration or pathology
- Rate of _____ or _____ by liver or kidney (ie renal failure -> rate of elimination decreased -> increased concentration)
- Alterations in how target cells _____ to the hormone such as?
Takeaway: Any endocrine disorder that affects target cell’s ability to bring about physiological response =
- activation or elimination
- respond (ie lack of expression of receptors, receptors that are dysfunctional, receptor expression increased)
= dysfunction in feedback regulation
Hypothalamus and Pituitary Glands (Central Endocrine Glands)
Hypothalamus connected to
(1) through neurological extension (cell bodies in hypothalamus, travel down connecting stalk, and axon terminals sit in this structure)
(2) Hormones released
(1) completely separate gland from hypothalamus (majority of mass of pituitary is in this lobe)
(5) Hormones released
Posterior Pituitary
ADH, Oxytocin
Anterior Pituitary
TSH, ACTH, Prolactin, Growth Hormone, LH/FSH
Hormone (Notes)
Hormones released from posterior pituitary are actually produced by the ______, stored, and released by posterior pituitary -> therefore posterior pituitary is not a?
Hormones released by anterior pituitary -> hypothalamus releases hormone that acts on cells in the anterior pituitary to then release a different hormone
(1) -> (1) -> (1) that anterior pituitary hormone acts on
hypothalamus -posterior pituitary not a true endocrine gland just an extension of the hypothalamus
Hypothalamic hormone -> Anterior Pituitary Hormone -> Peripheral gland
Anterior Pituitary Hormone
TSH cycle
- Hypothalamic Hormone
- Anterior pituitary cell and hormone
- Peripheral gland and hormone
- TRH (Thyroid Stimulating Hormone)
- Thyrotrope cells, TSH
- Thyroid gland, T3, T4
ACTH Cycle
- Hypothalamic Hormone
- Anterior pituitary cell and hormone
- Peripheral gland and hormone
- CRH (Corticotropin Releasing Hormone)
- Corticotropes, ACTH
- Adrenal gland, Cortisol
Prolactin Cycle
- Hypothalamic Hormone
- Anterior pituitary cell and hormone
- Peripheral gland and hormone
- PRH (Prolactin Releasing Hormone) or PIH (Prolactin Inhibitory Hormone)
- Lactotropes, Prolactin
- Mammary glands, Breast milk production
PIH dominant most of the time except postpartum period
Growth Hormone Cycle
- Hypothalamic Hormone
- Anterior pituitary cell and hormone
- Peripheral gland and hormone
- GhRH (Growth Hormone releasing hormone) or Somatostatin (growth inhibiting hormone)
- Somatotropes, Growth Hormone
- Peripheral glands and hormones
- Liver -> insuline like growth factor 1 and 2
- All tissues -> growth of all tissues (esp visceral organs and lean muscle mass)
FSH/LH Cycle
- Hypothalamic Hormone
- Anterior pituitary cell and hormone
- Peripheral gland and hormone
- GnRH (Gonadotropin Releasing Hormone)
- Gonadotropes, FSH and LH
- FSH -> ovaries and testes to produce gametes Sperm and Ova, LH -> ovaries and testes to produce estrogen/progesterone and testosterone
Feedback Regulation
=
Every target hormone released provides negative feedback at both the level of the Anterior Pituitary and Hypothalamus
ie) T3 and T4 inhibits both TSH and TRH, breast milk thats not emptied from breasts inhibits prolactin and PRH
ADH
=
- Regulated based on plasma ______
- Normal plasma osmolarity = _____mOsm
- Increase in plasma osmolarity = _____ secretion of ADH (very _____ relationship: 1% increase in osmolarity = 1% increase in ADH secretion)
- Minimum threshold for release of ADH = ____mOsm
- <280mOsm = ADH concentration is ___ (if your plasma is dilute you don’t want to retain water)
Acts on collecting ducts of kidneys and causes water retention
- osmolarity
- 290mOsm
- increase (linear relationship)
- 280mOsm
- 0
Syndrome of Inappropriate ADH secretion (SIADH)
=
- Means that person is releasing ADH for _____ reasons than plasma osmolarity or some alteration in the _____ of the system
Too much ADH than is normal for that person’s plasma osmolarity
(Higher ADH concentration for any given value of osmolarity)
- different reasons than plasma osmolarity or alteration in sensitivity of the system
SIADH Causes
(6)
Increased Hypothalamic Production
Pulmonary Diseases
Severe Nausea and/or Pain
Ectopic Production of ADH
Drug induced potentiation of ADH
Idiopathic
Increased Hypothalamic Production
(3) (2) (2)
Infections (meningitis, ecephalitis, etc)
Neoplasms (tumors in hypothalamus)
Drug induced (chemotherapies, antipsychotics)
Pulmonary Diseases
(4)
Theory =
Pneumonia, Tuberculosis, ARF, Asthma
Compensatory mechanism to expand plasma volume when you have chronic hypoxia (not well understood though)
Severe Nausea or Pain
=
Ectopic Productions (3)
=
Drugs
=
Intensely stimulates SNS which in turn stimulates ADH
Oat cell of Lung
Bronchogenic Carcinoma
Carcinoma of Duodenum
Some group of cells that now produce a hormone that shouldn’t be there (malignant cells) -> v dangerous bc unlike normal endocrine glands has no regard for feedback mechanisms
Some drugs increase sensitivity of collecting ducts and distal tubules to ADH to increase effects
Clinical Manifestations of SIADH
- Serum ______ and ______
- Urine ______
- Urine sodium excretion that _____ sodium intake
- Normal ____ and _____ function
- ______ of conditions that can alter ____ status (like (2), etc)
- Serum hypoosmolarity and hyponatremia (low plasma osmolarity <290mOsm)
- Urine hyperosmolarity urine will be concentrated
- matches
- adrenal and thyroid
- Absence, volume (CHF, renal insufficiency)
Opposite directions of plasma osmolarity vss urine = we know there’s a problem in the ADH system
3, 4, 5 about ruling out other problems
4 Types of Osmoregulatory Defects
(4)
Type A (Random)
Type B (Reset Osmostat)
Type C (Leak)
Type D (Decreased renal sensitivity)
Type A (Random)
Observed in __%, large and _____ fluctuations in AVP occur unrelated to?
Usually occurs in association with ______
- Normally, plasma osmolarity drives changes in ADH, but in this random type you see (1) drive changes in (1)
- Cause: this pattern matches _____ productions of ADH - consequence is?
20%, unrelated fluctuations in AVP unrelated to plasma osmolarity
Tumors
- flucutations in AVP drive changes in osmolarity
- Ectopic production -> no feedback regulation, cancer is releasing as much ADH as it wants
Type B (Reset Osmostat)
Observed in about __%, a prompt and _____ rise in AVP with plasma osmolarity, but a significant _____ of the _____ for release is present.
Pattern consistent with an osmoreceptor _____ at a ____ than normal level (from _____ disorders)
35%, parallel, lowering of threshold
reset at a lower than normal level (pulmonary disorders)
Instead of 280mOSm, will be 260mOsm - so start to see ADH at osmolarity lvls lower than you expect (shift in the settngs in the range)
Still a linear relationship just threshold has been reset
Causes: consistent in SIADH caused by pulmonary disorders
Type C (Leak)
=
Cause
Observed in 35%, AVP is persistently elevated at low and normal plasma osmolarity, however, above the threshold for AVP release, plasma AVP increases normally.
Meningitis or Head injuries
responsiveness is still normal, ie 280mOsm threshold, however even below 280mOsm, you have persistent leaking of ADH
Type D (Decreased Renal Sensitivity)
=
Causes
Observed in 10% plasma AVP is appropriately suppressed under hypotonic conditions and does not rise until plasma osmolarity reaches the normal threshold level: it does not result in maximal urinary dilution.
Increased renal sensitivity to vasopressin, like when your on drugs
Increased sensitivity to ADH like when your on drugs
Diabetes Insipidus Name
The word diabetes is derived from Greek word diabainein, which means?
Insipidus comes from a Latin word meaning?
Means to stand with legs apart, as in urination
means without taste
When they tasted urine and it was sweet = diabetes mellitus
Diabetes Insipidus
Central DI =
Nephrogenic DI =
- Characterized by the excretion of ____ volumes of ____ urine
- Patients have a partial or total inability to ______ urine
- Urine output can be anywhere from ____ or ____ L/day
A failure to secrete ADH, problem is coming from CNS, hypothalamus’s ability to produce ADH
A failure to response to ADH, problem is the kidneys
- large, dilute
- inability to concentrate urine
- 4-8 to 8-12L/day
Most dilute from last unit is about 100mOsm
Diabetes Insipidus Nongenetic Causes
Typical injuries include (3)
At all ages, destructive lesions of the (2) are the most common cause of DI
Head trauma, Tumor, Neurosurgical procedures
Pituitary and/or Hypothalamus
Diabetes Insipidus Genetic Causes
(4)
Genetic causes ____ Central and Nephrogenic DI (dont’ have to memorize all)
Once cause of Nephrogenic DI is an ___ linked disorder (more commonly effects males), more common in european countries, esp Irish
- CDI with an autosomal pattern inheritance is dt a mutation in the prepro-arginine vasopressin (prepro-AVP2) gene
- CDI with DM, optic atrophy, and mental retardation (Wolfram syndrome) may be inherited in an autosomal recessive pattern
- X linked NDI occurs from mutations in the antidiuretic arginine vasopressin V2 receptor (AVPR2) gene, mapped to Xq28
- NDI with an autosomal dominant or recessive pattern is due to mutations in the gene designated AQP2, this gene directs water channel formation in the distal tubule
both
X linked disorder
Lab Values for Pts with Diabetes Insipidus
- Plasma osmolarity =
- Urine osmolarity =
- Plasma ADH in Central DI =
- Plasma ADH in Nephrogenic DI =
- Elevated
- Very low, dilute urine
(we don’t have or can’t respond to ADH so we can’t concentrate urine so very dilute urine and losing water so very concentrated plasma)
- Decreased
- Normal or High bc body is still releasing ADH but kidneys can’t respond to it
Psychogenic DI
AKA Psychogenic ______
=
Psychogenic Polydipsia
In times of mania or acute delusion/schizophrenia, individuals sometimes have intense polydipsia where they have unquenchable thirst and consume huge volumes of water
Behavior is what causes the problem not the system
Diabetes Insipidus Treatments
Central DI (1)
Nephrogenic DI (3)
- Desmopressin (synthetic form of Vasopressin (ADH))
- Thiazide diuretic (counterintuitive bc you have polyuria but trying to get a side effect of the drug, where you increased water reabsorption at proximal tubules)
- Vigilant Hydration
- Minimize water loss through physical activity
Diseases of the Anterior Pituitary
Hypopituitarism
- Pituitary _____
- ______ Syndrome
- ______ Hypopituitarism
- Tr_____
- I_______ Diseases
- G______ Abnormalities of Pituitary Development
- _____ Hormone Insensitivity (Laron Syndrome)
- Tumors (Adenomas)
- Sheehan
- Iatrogenic
- Trauma
- Infiltrative
- Genetic
- Growth
Disease of Anterior Pituitary
Hypopituitarism (Notes)
- Adenomas =
- Sheehan Syndrome =
- Iatrogenic =
- Infiltrative diseases (2)
- Laron Syndrome =
- Benign overgrowth of pituitary tissue
- All pituitary hormones are low or lacking, complication of postpartum hemorrhage, in pregnant women, their anterior pituitaries get much larger so oxtgen demand of the gland goes up -> prone to ischemia -> after postpartum hemorrhage -> ischemic damage to pituitary gland
- from medical care (neuro surgeries cause damage to pituitary gland)
- Meningitis, Encephalitis
- Where ppl have primary insensitivity to growth hormone - where target cells have defective or lacking receptors
Most Common Cause of HYPO and HYPER pituitary disorders
=
Hyperpituitarism =
Hypopituitarism =
Adenomas - benign overgrowth of pituitary tissue
overgrowth of different types of anterior pituitary tissue
when adenomas get too large can damage pituitary gland when it grows outside its bony encasement -> compression of gland against other structures damages cells
Hyperpituitarism - Pituitary Adenomas
Are classically classified histologically according to their staining properties:
- (1) - associated with oversecretion of GH
- (1) - associated with oversecretion of ACTH
- (1) - no endocrine hyperfunction
Now more regularly clasfied based on the _____ they secrete
Microadenomas =
Macroadenomas =
- Acidophil
- Basophil
- Chromophobe
hormone
<10mm in diameter
>10mm in diameter
Hyperpituitarism Pituitary Adenomas
Manifestations based off 2 questions
-
(1)
- If yes, will have a spectrum of ____ rt _______
-
(1)
- If it is a ____adenoma, will also cause other problems such as? (2)
- Does this adenoma oversecrete hormone?
- S/S rt oversecretion
- Is this a micro or macroadenoma?
- Impingement on other structures in brain by outgrowing bony encasement -headaches, blurry vision from optic nerve impingement
Hyperpituitarism - Pituitary Adenomas
(6)
Lactotrope Adenomas
Somatotrope Adenomas
Corticotrope Adenomas
Gonadotrope Adenomas
Thyrotrope Adenomas
Nonfunctional Pituitary Adenomas
Lactotrope Adenomas
aka ____omas
How common?
Tend to be micro or macro?
- In females (3)
- In males (2)
Prolactinomas (oversecrete prolactin)
Most common
Microadenomas
- Amenorrhea (loss of menstruation), Galactorhea (milk production), Infertility
- Decreased libido, Erectile dysfunction
Somatotrope Adenomas
Oversecretes (1)
75% are ____adenomas
- Consequence depends on ___ of onset
- Childhood =
- Post puberty =
Growth hormone, and can cause other problesm bc usually a
Macroadenoma
- Age
- Gigantism (#1 cause)
- Acromegaly
Corticotrope Adenoma
Produces excess _____
Usually a ____adenoma
Can cause (1) Syndrome
ACTH -> Cortisol
Microadenoma
Cushing’s
Gonadotrope Adenoma
Secrete (2)
Tend to be _____adenomas
FSH, LH
Macroadenomas
Thyrotrope Adenomas
How common?
Over secretion of ____
Rare
TSH
Nonfunctional Pituitary Adenomas
=
- ____ cell adenomas
- ____cytoma
- S_____ Adenomas
Don’t oversecrete hormone so just causes S/S based on how large they get
- Null cell adenomas
- Oncocytoma
- Silent Adenomas
Somatotrope Adenomas
Hypersecretion of _____ hormone
- ______ vs. ______
- Increased GH and _____ like growth factor (IGF)
- In children: increased growth in (1)
- In adults: causes increased proliferatio in _____ tissue, c_____ matrix, and increased ____ growth
- Metabolic effects
- ______ metabolic rate, GH _____ of glucose uptake and _____ hepatic production of glucose (____glycemia)
- Increased risk of (1)
Growth
- Acromegaly vs. Gigantism
- GH + Insulin like growth factor
- long bones
- connective, cytoplasmic, bony
- Metabolic effects
- Increased metabolic rate, GH inhibition of glucose uptake and increased hepatic production of glucose (hyperglycemia)
- Diabetes Mellitus
Why do you not see Gigantism with Somatotrope adenomas in adulthood?
Bc around puberty you have a _____ off of (1) of long bones
- Before puberty those growth plates are mostly?
- Around puberty these plates become?
Acromegaly - can’t get longer but you can get a _____ of bones and increase in _____ tissue production
sealing off of growth plates
- cartilage and continue to elongate
- ossify and become bone so can no longer elongate
thicker, and increase in connective tissue
GH and Insulin Like Growth Factor
With an increase in GH?
- GH has what effect?
- Insulin like growth factor has what effect?
Depending on balance of these two hormones =
You also see an increase in insulin like growth factor
- anti-insulin effects
- insulin effects
Increased risk for DM
Acromegaly Characteristics
- Prominent ____ ridge
- Bone of j__ and ch___ thicker
- Subcutaneous tissue -> large _____ face
- _____ gland enlargement
- Enlarged h_____
- ____tension
- Inappropriate _______ in females
- Impaired _____ tolerance or ___
- brow
- jaw, chin
- puffy face
- Thyroid
- hearts
- Hypertension
- lactation
- impaired glucose tolerance or DM
Thyroid Conditions
(3)
HPT axis = Hypothalamic hormone (1) -> Anterior pituitary hormone (1) -> Thyroid gland hormones (2)
- Feedback regulation at levels of both (1) and (1)
- Hyperthyroid
- Hypothyroid
- Euthyroid (normal thyroid levels)
TRH -> TSH -> T3, T4
hypothalamu and anterior pituitary
Non Toxic Goiters
Almost always a ______ condition
Something is going on to cause excessive thyroid growth but plasma thyroid hormone levels are ______ = “non toxic”
- Problem stems from thyroid gland itself: inefficiency in production of T3, T4 from either (2)
- Bc it has difficulty producing T3, T4, compensatory mechanisms?
- Levels of TRH, TSH, T3, T4 =
So what increases the cellularity and size of the thyroid gland cells?
Euthyroid
Normal (if rise above normal can become toxic)
- Decreased sensitivity to TSH or decreased ability to produce T3, T4
- Anterior pituitary secretes excess TSH to compensate
- Elevated TRH, Elevated TSH, Normal T3 T4
Increased TSH stimulates thyroid growth
Hypothyroidism
=
Causes of Primary Hypothyroidism
(6)
Thyroid hormone deficiency
- Autoimmune (Hashimoto Thyroiditis)
- Postradioactive iodine therapy for hyperthyroidism
- Total or subtotal thyroidectomy
- Radiation therapy for head/neck ca and lymphoma
- Iodine deficiency
- Congenital disorders of thyroid hormone synthesis
Radioactive iodine kills off excess thyroid tissue -> overdose can kill off too much and cause hypothyroidism
Iodine is the only component of thyroid hormone that our body cannot synthesize, so inadequate dietary intake -> hypothyroidism
Hypothyroidism
Other Causes
- Iodine _____
- Certain drugs (3)
- Diseases of the ______
- Excesses (too much iodine is toxic, has a range)
- Lithium, Interferone alpha, some Antiepileptic drugs (drugs that interfere production of thyroid hormone)
- Hypothalamus
Hashimoto Thyroiditis
=
Autoimmune disorder where person’s immune system is producing autoreactive T and B cells - autoreactive to antigens on thyroid gland cells -> T cell and B cell attack of thyroid cells/tissue
Graves Disease
=
- The antibody in Graves acts as a (1) - mimics its action therefore is named (1)
- B cells combine to the TSH receptor and ______ the TSH receptor instead of mounting an attack
- Also acts as a ____ factor that stimulates the ___ of the thyroid gland -> so will also see a ____
Is there anyting regulating TSI?
Autoimmune disorder that is a type II hypersensitivity disorder where you produce inappropriate antibodies that binds to self antigens
- TSH agonist - Thyroid Stimulating Immunoglobulin (TSI)
- stimulate
- growth, size, goiter
NO - stimulates thyroid gland without caring about the outcme so significant production of T3 T4 -> feedback loop will suppress TSH and TRH
Hypothyroidism Clinical Manifestations
- _____ from excess TSH
- Reduced metabolic rate causes
- Chronic f_____
- Muscle ____
- ____ intolerance
- Difficulty maintaining/losing ____
- Hair is _____, _____
- F_____ problems
- Skin is ____
- Particular type of edema (1)
- Seen in what parts of the body? Severe complication (1)
- Goiter
- Reduced metabolic rate
- fatigue
- weakness
- Cold
- Weight
- Coarse, brittle
- Fertility
- Pale
-
Myxedema: extracellular edema from increase in production of connective tissue, is not fluid accumulation, is a puffiness caused by increase in tissue
- Hands, face, tissues in brain and heart -> Myxedema Coma
Hyperthyroidism
=
General Causes
(3)
Most common cause =
Excess amounts of circulating thyroid hormone
- Presence of abnormal thyroid stimulator (graves disease)
- Intrinsic disease of thyroid gland (toxic multinodular goiter or functional adenoma)
- Excess production of TSH by anterior pituitary (rare) - by thyrotrope adenoma
Graves Disease
Hyperthyroidism Manifestations
- _____ energy, Ag_____, ____ up person
- Excess Metabolism
- Muscle _____, S_____
- _____ menstrual cycles in females
- HR is _____
- G______
- Profuse sw_____
- Hand _____
- Eyes (1)
- Nervous, Agitated, Hyped up
- Excess Metabolism
- Muscle wasting, Skinny
- Abnormal
- Tachycardia
- Goiter
- Sweating
- Tremors
- Exophthalmos -> protruding eyes dt retroorbital edema
Addison Disease
=
- Primarily ______ destruction of adrenal tissue
- Affects both (2) function
Adrenal Cortical Insufficiency
- Autoimmune
- Glucocorticoids (cortisol), Mineralcorticoids (aldosterone)
Addison’s Disease Effects
- Hyper_______ (excess ACTH on _____)
- Progressive w_____, fatigue, poor _____, and weight _____
- D_____ with orthostasis dt hypotension occasionally may lead to ______ (____ depletion)
- ____natremia and ____kalemia
- ____ craving
- Hyperpigmentation (melanocytes)
- weakness, appetite, loss
- Dizziness, syncope (volume depletion)
- Hponatremia, Hyperkalemia
- Salt
Adrenal Crisis
=
Brought about by ____ stress (ie s_____, sur____ stress) in absence of adrenal cortex hormones stress results in h_____, sh____, an risk of _____
Cannot mobilize a stress response when needed for acute stress
acute stress (sepsis, surgical stress) -> hypotension, shock, risk of death
Addison Disease Effects (Notes)
- Excess ACTH sitmulates melanocytes -> ppl will have _____ of abnormally dark skin (not uniform, will be _____ splotches)
- Weight loss dt lack of ____ gluco and mineralcorticoids
- Debilitating d_____
- Most significant effects that ppl experience are from loss of _____corticoid (1) -> v difficult time regulating (2) -> weakness, fatigue, orthostatic hypotension, difficulty maintaining BP, chronic hyponatremia (salt cravings), hyperkalemia
- patches (not uniform, scattered splotches)
- both
- dizziness
- mineralcorticoid (Aldosterone) -> sodium and potassium
Cushing’s Syndrome
=
Cushing syndrome is caused by prolonged exposure to _____ levels of either _____ or _____ ______
Prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids
Cushing’s Syndrome Causes
- Exogenous _____ Administration
- Patients with diseases that respond to _____ therapy (1)
- Patients who have undergone (1)
- Endogenous _____ overproduction
- ACTH-producing (1)
- Primary _____ lesions
- (2)
- _____ ACTH production
- Steroid
- steroid (prednisone)
- organ transplants
- Glucocorticoid
- pituitary adenoma
- Adrenal lesions
- Adrenal adenomas, carcinomas
- Ectopic (Malignant tumors usually from lung carcinomas that overproduce ACTH)
Cushing’s Syndrome Clinical Manifestations
Cortisol Functions
- Is an _____ suppressant
- Difficult to ____, more prone to ____ breakdown
- Is a ____corticoid (increases BG, antagonizes insulin)
- Ppl will be ______ -> temporary type II ___ state (excess urination, dehydration)
- Usually stimulates central _____ -> increases deposition of fat in _____ viscera and f____
- Ppl will have fact accumulation in (3)
- Decreased deposition in fat everywhere else (2)
- Immune suppressant
- heal, skin breakdown
- Glucocorticoid
- Hyperglycemic, type II DM state
- Central adiposity, abdominal viscera and face
- face, belly, back (buffalo hump)
- skinny legs and arms
Cushing’s Syndrome Clinical Manifestations
Cortisol Functions cont.
- Cortisol usually has mild _____ effects -> tends to promote sodium _____ and potassium _____
- ___natremia, ___kalemia
- Cortisol ______ bone
- ______ condition
- Cortisol usually increases _____ agility but if it gets too high
- Ppl become emotionally _____, m_____, and VERY EASILY ______
- aldosterone -> Na retention, K secretion
- Hypernatremia, Hypokalemia
- Demineralizes bone
- Osteoporosis
- Mental agility
- Labile, moody, AGITATED
Cushing’s in Females
Will create a significant change in facial features
- Cheeks =
- _____ hair
- Face and neck =
- Increased ___ deposition in face and ____
- High chipmunk
- Facial hair
- Flushed red
- Fat in face and back
