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Pathophys 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the role of endocrine glands?

A

To release chemical messengers directly into the bloodstream

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2
Q

Three different types of chemical hormones

A

o Peptide hormones
o Amino acid derived hormones
o Steroid hormones

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3
Q

Effectiveness of a hormone depends on whether the hormone is (2)

A

FREE and BIOLOGICALLY AVAILABLE

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4
Q

What do we mean when we say that a hormone needs to be “free”?

A

We mean “not bound to a plasma protein.” (which lipid soluble vitamins need to do to travel in the blood

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5
Q

What do we mean when we say that a hormone needs to be “biologically available”?

A
  • Activation may occur in bloodstream, eg angiotensinogen → interacts with rennin to become angiotensin I → ACE
  • Activation may be carried out by the liver
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6
Q

What is hormonal regulation? Depends on…

A

o Rate of absorption of hormone (drain)

o Rate of elimination of hormone (faucet)

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7
Q

How does hormonal feedback regulation work?

A

Negative feedback system to original gland

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8
Q

What is the role of specific hormone binding proteins?

A

o Help facilitate the hormone’s tendency toward creating long term actions (extends half-life)

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9
Q

Two locations of hormone receptors

A

o Surface receptors on the membrane (Second messenger system involved)
o In the nucleus – on the promoter region (typical of steroid hormones)

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10
Q

Sources of alterations in endocrine function (6)

A
  • Hormone secretion
  • Less Hormone Binding → Higher concentration of free hormone
  • Altered rate of elimination: Liver or Kidney problems
  • “Hormone Resistant Conditions”: Failure of target cell to respond to hormone:
  • Autoimmune problem with endocrine cell = primary deficiency of that hormone
  • Pituitary Gland and Alterations in Function
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11
Q

What may cause a hypersecretory problem (hormones) (2)

A
  • May be due to adenoma – overgrowth of endocrine tissue

* Ectopic production: Cancer cells may oversecrete hormones –>No feedback regulation

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12
Q

What may cause less hormone binding?

A

o May be caused by liver problem, plasma protein / albumin deficiency
o Affects rate at which the hormone binds to the target cell, gets eliminated.

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13
Q

What may cause altered rate of elimination?

A

o Liver or kidney problems: Some hormones need to be biotransformed by liver, excreted by kidneys

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14
Q

What occurs in “hormone resistant conditions?” Which is the most common?

A

Target cell fails to respond to hormone.

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15
Q

Three types of hormone resistant conditions. Which is the most common?

A
  • **Receptor associated disorders
  • Intracellular disorders
  • Feedback regulation becomes altered

(Receptor associated disorders = most common)

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16
Q

What occurs with receptor associated disorders? What type of hormone does this most often happen to?

A
  • Rate of receptor expression may be decreased or sensitivity decreased
  • Mostly lipid soluble hormones
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17
Q

Two examples of autoimmune problems with endocrine cells.

What occurs?

A

o Diabetes mellitus Type 1
o Hashimoto Thyroiditis (Hypothyroidism)

Primary deficiency of that hormone

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18
Q

Alterations to the pituitary gland: Posterior lobe

  • How common?
  • How is this associated with the hypothalamus?
  • What are the cell types?
  • What are the hormones produced? (2)
A
  • 10% of pituitary masses?
  • Neurological extension of the hypothalamus
  • Axon terminals of the neurosecretory neurons in the PVN and SON of the hypothalamus
  • Vasopressin (ADH), Oxytocin
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19
Q

Alterations to the pituitary gland: Anterior lobe

  • How common?
  • How is this associated with the hypothalamus?
  • What are the cell types?
  • What are the hormones produced? (2)
A
  • 90% of pituitary masses
  • Hypothalamic tropic hormones act on these cells to stimulate other hormone release
  • Contains glandular cells arranged in nests surrounded by dense vascular tissue
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20
Q

What are the hypothalmic tropic hormones (5)? What is their role?

A
  • Corticotropes – secrete ACTH
  • Lactotropes – secrete prolactin
  • Somatotropes – secrete GH – constitute half of all hormone-producing cells in the anterior lobe
  • Thyrotropes – secrete TSH (5% of all cells in the AP)
  • Gonadotropes – secrete FSH and LH

(All stimulate endocrine glands except prolactin – stimulates excretory gland)

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21
Q

What are 2 examples of a hypersecretory disease of the posterior pituitary?

A
  • Syndrome of Inappropriate ADH secretion (SIADH)

- Diabetes insipidus

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22
Q

What is SIADH? Def

A

Syndrome of Inappropriate ADH:

  • High levels of ADH in the absence of normal ADH secretion stimuli
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23
Q

What happens to osmolarity with SIADH? What happens to urine?

A

ADH levels are high, plasma osmolarity low (dilute): TOO MUCH WATER RETAINED, urine very concentrated.

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24
Q

SIADH: Causes (6)

A
  • Increased hypothalamic production
  • Pulmonary diseases
  • Severe nausea and/or pain
  • Ectopic production of AHD
  • Drug induced potentiation of AHD
  • Idiopathic
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25
Q

What can cause increased hypothalamic production (ultimately resulting in SIADH)?

A
  • Infections (meningitis, encephalitis, etc)
  • Neoplasms
  • Drug-induced (chemotherapeutics, antipsychotics)
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26
Q

What pulmonary diseases can result in SIADH (4)?

What is the mechanism?

A
  • Pneumonia
  • Tuberculosis
  • Acute Respiratory Failure (ARF)
  • Asthma

**Mechanism unclear; could be compensatory

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27
Q

Why would severe nausea and/ or pain trigger SIADH?

A

Due to SNS stimulation, which triggers ADH

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28
Q

3 ectopic causes of SIADH

A
  • Small cell / oat cell carcinoma of the lungs
  • Bronchogenic carcinoma
  • Carcinoma of duodenum
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29
Q

Clinical manifestations of SIADH (2)

A

(1) Serum hypoosmolarity and natremia

(2) Urine hyperosmolarity

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30
Q

What are three other clinical manifestations of SIADH (noted to r/o other disorders)?

A

(1) Urine sodium excretion matches sodium intake
(2) Normal adrenal and thyroid function
(3) Absence of conditions that can alter volume status (Coagulative heart failure, Renal insufficiency)

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31
Q

Four distinct types of osmolaregulatory defects and their prevalence (%)

A

TYPE A: Random (20%)
TYPE B: Osmostat reset (~35%)
TYPE C: Leak (35%)
TYPE D: renal insensitivity (10%)

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32
Q

Describe what occurs in Type A osmoregulatory Disorders

A

RANDOM

Large and unrelated fluctuations in ADH (aka AVP) occur unrelated to the rise of plasma osmolarity

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33
Q

Describe what occurs in Type B osmoregulatory Disorders

A

OSMOSTAT RESET

Prompt and parallel rise in AVP with plasma osmolarity, but a significant lowering of the threshold for release is present

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34
Q

Describe what happens in Type C osmoregulatory disorders

A

LEAK

ADH (AVP) is persistently elevated at low and normal plasma osmolarity. Above the threshold for AVP release, AVP increases normally.

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35
Q

Describe what occurs in Type D osmoregulatory Disorders

A

RENAL INSENSITIVITY

Plasma ADH (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.

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36
Q

Type A Pattern

A

Usually occurs in association with tumors

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37
Q

Type B Pattern

A

Consistent with an osmoreceptor reset at a lower-than-normal level (pulmonary disorders)

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38
Q

Type C Pattern

A

Observed in meningitis, head injuries

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39
Q

Type D Pattern

A

Consistent with an increased renal sensitivity to vasopressin

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40
Q

Treatments for osmoregulatory defects (2)

A
  • Fluid restriction

- V2 (vasopressin) receptor blockers

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41
Q

Diabetes insipidus is characterized by what?

A

The excretion of large volumes of dilute urine, having nothing to do with plasma glucose

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42
Q

What are the two types of Diabetes Insipidus?

A
  • Neurogenic (or central): Failure to produce ADH

* Nephrogenic (renal): Failure to respond to ADH

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43
Q

What is the most common cause of DI at all ages?

A

Destructive lesions of the pituitary and/or hypothalamus

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44
Q

What causes neurogenic diabetes insipidus (3)

A
  • Head trauma
  • Tumor
  • Neurosurgical procedures
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45
Q

What is going on genetically with nephrogenic diabetes insipidus?

Type of Inheritance

A
  • CDI with an autosomal dominant pattern inheritance
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46
Q

What three disorders may be linked to an autosomal recessive pattern associated with Diabetes Insipidus?

A
  • Diabetes Mellitus
  • Optic atrophy
  • Mental retardation (Wolfram syndrome)
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47
Q

What is going on genetically with nephrogenic diabetes insipidus?

Mutation of what gene? (name 4…?!)

A
  • Due to a mutation in the prepro-arginine vasopressin (prepro-AVP2) gene
  • X-linked NDI occurs from mutations in the antidiuretic arginine vasopressin V2 receptor (AVPR2) gene, mapped to Xq28

• NDI with an autosomal dominant recessive pattern is due to mutations in the gene designated to AQP2; this gene directs water channel formation in the distal tubule.

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48
Q

Clinical manifestations of DI

A
  • Polyuria:

* Polydipsia

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49
Q

Polyuria in diabetes insipidus

2 characteristics

A
  • Massive amount of dilute urine (little to no ability to concentrate urine = plasma osmolarity 500 mOsms)
  • Insipidus = “without taste” (in DM, urine tasted sweet)
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50
Q

Why does a DI patient suffer polydipsia?

A

• Extreme thirst, because plasma is always hyperosmolar

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51
Q

How do the lab values for Diabetes Insipidus compare to the lab values of SIADH?

A

MIRROR IMAGE.

In DI, plasma osmolarity is concentrated / urine osmolarity is dilute (low specific gravity)

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52
Q

What type of Diabetes insipidus is easier to treat? Why?

A

Central DI is easier to treat

For Central DI, just administer synthetic ADH. For Nephrogenic DI, Kidney is no more sensitive to synthetic ADH than it is to natural ADH

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53
Q

Treatment for central DI

A

Administer synthetic ADH

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54
Q

Treatment for Nephrogenic DI

A
  • Restrict physical activities to prevent water loss
  • Vigilant hydration
  • Paradoxically, thioside diuretics can be used for tx
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55
Q

Why are thyoside diuretics an effective treatment for nephrogenic DI?

A

Increases sodium loss → Decreases hypernatremia

56
Q

Diseases of the anterior pituitary (3)

A
  • Hypopituitarism
  • Hyperpituitarism
  • Hypersecretion of GH
57
Q

What do adenomas of pituitary cells cause?

A

Can cause either hypo- or hyper- thyroidism

Either crushes the gland or causes hypersecretion

58
Q

What is panhypopituitarism?

A

A total failure of pituitary function.

59
Q

What can cause disorders of the anterior pituitary? (7)

A
  • Adenomas (Pituitary Tumors)
  • Sheehan Syndrome:
  • Iatrogenic Hypopituitarism
  • Trauma
  • Infiltrative Diseases
  • Genetic Abnormalities of Pituitary Development
  • Growth Hormone Insensitivity: Laron Syndrome
60
Q

How can an adenoma cause hypopituitarism in the anterior pituitary?

A

• Pituitary adenoma crushes pituitary gland against the turca selcia (Bone) → Causes injury to secretory cells → Decline in pituitary secretions.

61
Q

How can Sheehan syndrome cause hypopituitarism in the anterior pituitary?

A

• During pregnancy, pituitary gland bulks up → Increased oxygen demands → Becomes vulnerable to ischemia → Ischemic damage occurs with hemmhorage

62
Q

What is Sheehan Syndrome?

A

A complication of postpartum hemmorhage

63
Q

When might an iatrogenic hypopituitarism occur?

A
  • Inadvertently caused by medical intervention

* Due to neurological surgery that causes direct damage or increased ICP

64
Q

What is an example of an infiltrative disease that might cause hypopituitarism?

A

Meningitis

65
Q

What is Laron Syndrome?

  • Physiologically
  • Clinically. Why?
A

Primary insensitivity to growth hormone: Adequate GH is produced, but GH receptors are impaired.

Result: Person has proportional body, but small stature. B/c growth hormone is necessary for bone elongation

66
Q

How are pituitary adenomas classified? List (3)

A

According to their staining properties
• Acidophil
• Basophil
• Chromophobe

67
Q

Acidophil pituitary adenoma: effects on endocrine function (2)

A
  • Associated with oversecretion of GH

- Now more regularly classified by what they secrete

68
Q

Basophil pituitary adenoma: effects on endocrine function

A

– associated with oversecretion of ACTH

69
Q

Chromophobe pituitary adenoma: effects on endocrine function

A

– no endocrine hyperfunction

70
Q

How does size impact the effect of pituitary adenomas?

A
  • Adenomas less than 10mm in diameter (microadenomas) do not cause symptoms unless they produce hormone
  • Larger Pas (macroadenomas) cause local symptoms (impinging on other structures) and systemic symptoms b/c of hormone oversecretion
71
Q

Types of pituitary adenomas (5)

Which is the most common?

A
  • Lactotrope Adenoma (prolactinomas) –> most common
  • Somatotrope adenomas
  • Corticotrope Adenoma
  • Gonadotrope Adenoma
  • Thyrotrope Adenomas
72
Q

Types of nonfuncitonal pituitary adenomas (3)

A
  • Null cell adenomas
  • Oncocytoma
  • Silent Adenomas
73
Q

• ___% of all pit tumors removed surgically do not secrete excess hormone

A

25

74
Q

What are null cell adenomas?

A

o Chromophobic cells that test negative for all hormones

75
Q

What are oncocytomas?

A

o Similar to null cell but with higher mitochondrial density

76
Q

What are silent adenomas?

A

o Test positive for ACTH and sometimes other hormones as well – but never secretory

77
Q

Macroadenomas: Symptoms (4)

A
  • Visual disturbances, blurry vision, loss of parts of the field of vision
  • Headaches (chronic)
  • Increased ICP → Seizure
  • Impinge on hypothalamus → Problems with regulating bladder function, temp, plasma osmolarity
78
Q

Hypersecretion of growth hormone: Clinical manifestation (2)

A
  • Acromegaly in adults

- Gigantism in children

79
Q

Why are the clinical manifestations of excess GH different for children verses adults?

A

• Cartilage epiphysis seals off at puberty (because of sex hormones)

80
Q

Characteristics of a patient with acromegaly (6)

A
  • Increase in soft tissue: Enlarged hands, feet, nose, lips, ears.
  • Skin will seem much thicker
  • Pronounced brow ridges
  • Thick, protruding lower jaw (teeth of lower jaw look like they have gaps)
  • Enlargement of some internal structures (cardiomegaly – decreases contractility)
  • Thickening of vocal cords (very deep voice)
81
Q

Metabolic effects of excess GH (4)

A
  • Increased metabolic rate
  • Hyperglycemia from GH inhibition of glucose uptake in peripheral tissue
  • Increased hepatic production of glucose
  • This often leads to a compensatory hyperinsulinism and finally insulin resistance (DM2)
82
Q

What else increases with GH?

A

Insulin-like growth factor

83
Q

Complication of Hypersecretion of GH

A

Macro adenomas

84
Q

Treatment for hypersecretion of GH

A

OCTRIOTIDE

A somatostatin; decreases GH production

85
Q

Diseases of the thyroid gland (3)

A
  • Nontoxic goiter: Euthyroidism
  • Hypothyroidism (Hashimoto Thyroiditis)
  • Hyperthyroidism (Grave’s)
86
Q

Diseases of the adrenal cortex (3)

A
  • Congenital adrenal hyperplasia (CAH)
  • Adrenal cortical insufficiency (Addison)
  • Adrenal hyperfunction (Cushing)
87
Q

Define “Nontoxi goiter” / euthyroidism

A

The capacity of the thyroid to produce thyroid hormone (T3 and T4) is impaired / inefficient, so the body compensates by increasing TSH

88
Q

Elevated levels of TSH cause…

A
  • Normal T3 and T4

- Enlarged thyroid gland

89
Q

What is a nontoxic goiter in the early stages of the disease? Describe

A

DIFFUSE NONTOXIC GOITER

  • Gland is diffusely enlarged
  • Microscopically exhibits hypertrophy and hyperplasia of the epithelial follicular cells
90
Q

What is a nontoxic goiter as the disease evolves?

A

MULTINODULAR NONTOXIC GOITER

Can become a toxic goiter, which would be hypo/hyperthyroidism with a goiter

91
Q

Hypothyroidism is a consequence of what three general processes?

A

(1) Defective synthesis of thyroid hormone (with compensatory giotrogenesis)
(2) Inadequate function of thyroid parenchyma
(3) Inadequate secretion of TSH – by pituitary or of TRH by hypothalamus

92
Q

what causes inadequate function of thyroid parenchyma

A

usually a result of thyroiditis or surgical resection of the gland or the therapeutic administration of radioiodine

93
Q

What is the most common cause of primary hypothyroidism?

A

AUTOIMMUNE (Hashimoto thyroiditis)

94
Q

What happens in Hashimoto Thyroiditis?

A
  • Autoimmune destruction of thyrocytes (thyroid gland cells)
  • Both t-cell initiated destructino adn antibody-initiated destruction
  • High TSH, High TRH
95
Q

Possible causes of primary hypothyroidism (8)

A
  • Autoimmune
  • Postradioactive
  • Thyroidectomy (total or subtotal)
  • Radiation therapy for head / neck cancers and lymphomas
  • Iodine deficiency
  • Congenital disorders of thyroid hormone synthesis
  • Iodine excesses
  • Certain drugs
96
Q

What drugs might cause hypothyroidism?

A
  • Lithium – used to treat bipolar
  • Interferon alpha – abx
  • Some antiepileptic drugs
97
Q
  • What is Mike’s edema?

- What disease process is it concurrent with?

A
  • A non-pitting edema

- Hashimoto thyroiditis

98
Q

Mike’s Edema: Physiology

A

Accumulation of mucopolysaccharides attached to the extracellular matrix of tissues

99
Q

Mike’s edema: Clinical manifestations (5)

A
  • Enlargement in tongue, hands, tibial region (shin)
  • Appears like red bumpy plaques on skin
  • Puffiness in face
  • May enlarge heart
  • Altered mental status = Mike’s edema Madness
100
Q

Clinical manifestations of hypothyroidism

A
  • Fatigue
  • Feel cold + Cold extremities
  • Poor memory / concentration
  • Weight gain
  • Shortness of breath
  • Hoarse voice
  • Impaired hearing
  • Skin: Dry and coarse
  • Carpel tunnnel
  • Mike’s Edema
  • 3rd space fluid accumulation
  • Prolonged menstrual cycles
  • Goiter
101
Q

Why would a hypothyroid patient experience a goiter?

A

Excess TSH

102
Q

Signs and symptoms of hyperthyroidism reflect a _______ state

A

HYPERETABOLIC

103
Q

General causes of hyperthyroidism. Which is the most common?

A

(1) Presence of abnormal thyroid stimulator (graves disease)
(2) Intrinsic disease if the thyroid gland (toxic multinodular goiter or functional adenoma)
(3) Excess production of TSH by anterior pituitary (rare)

GRAVE’S is most common

104
Q

Mechanism of Grave’s (general)

A

Body produces an immunoglobulin antibody that attaches to the TSH receptor and acts as an antagonist to that receptor (activates it)

105
Q

Mechanism of Grave’s (more specific)

  • What is stimulated?
  • What is produced?
  • what is the result? (2)
A

o Ig antibody stimulates both thyroid hormone production and enlargement of the thyroid gland
o Immune system produces TSH agonist → High T3 & T4
o Because of elevated T3 and T4, less TRH and TSH are being produced
o Immune system is not part of regulatory loop; keeps stimulating the thyroid gland.

106
Q

Clinical manifestation of hyperthyroidism

A
  • Goiter
  • Exophthalamos: Extreme eye bulging (Due to retro-orbital swelling)
  • Irritable
  • Nervous
  • Jittery, constantly moving
  • Hand tremors
  • Difficulty sleeping
  • Thin looks thin and delicate
  • Weight loss (but good appetite)
  • Muscle wasting
  • Tachycardia
  • Increased sweating
  • Amenorhea, or Oligomenorhea (decreased frequency /duration)
107
Q

What hormones does the adrenal cortex produce? (Hint: This is review)

3 categories

A

1) Glucocorticoids
2) Mineral corticoids (Aldosterone)
3) Sex hormones

108
Q

What are the three types of glucocorticoids?

A

Cortisol
Cortisone
Corticosterone

109
Q

Of the adrenal hormones, which is the most devistating to lack?

A

Aldosterone

110
Q

Name 4 sex hormones

A
  • Androgens
  • Testosterone
  • Estrogen
  • Progesterone
111
Q

What causes Congenital Adrenal Hyperplasia (generally)?

A
  • A number of autosomal recessive enzymatic defects in the biosynthesis of cortisol from cholesterol
112
Q

A deficiency of ________ (enzyme) is responsible for ___% of CAH cases.

A

21-hydroxylase

90%

113
Q

What does a deficiency in 21-hydrogenase cause…

  • Chemically?
  • Physically? (2)
  • Diagnosis?
A
  • Causes lack of cortisol and the buildup of intermediates / increased production of androgens
  • Ambiguous genitalia is a direct result of the excess intermediates
  • Hyperplasia = a consequence of the lack of cortisol

DIAGNOSIS: CONGENITAL ADRENAL HYPERPLASIA

114
Q

Clinical manfestations of Congenital Adrenal Hyperplasia (not genitalia) - 2

A

• Small kidneys, massive adrenal glands (Hyperplasia due to lack of cortisol)

115
Q

o Cortisol provides negative feedback to:

A
  • The pituaitary gland and its production of ACTH.

* The hypothalamus and its production of CRH

116
Q

CAH: Affect on female genitalia

A
  • Exhibit pseudohermaphroditism (due to increased masculinization of genitalia in utero)
  • Fusion of the labia, an enlargement of the clitoris, shortened vaginal canal.
117
Q

1 cause of ambiguous genitalia in girls

A

CAH due to buildup of intermediates and an increased production of androgens

118
Q

CAH: Affect on male genitalia

A
  • Exhibit no abnormalities of the sexual organs

* May experience sexual precocity, stunted growth

119
Q

What is Addison’s disease?

A
  • Adrenocortical insufficiency due to the destruction or dysfunction of the entire adrenal cortex.
  • Primary autoimmune destruction of adrenal tissue
120
Q

What hormones does Addison’s disease affect?

A

• Affects both glucocorticoid and mineralocorticoid function.

121
Q

Adrenal cortical insufficiency (Addison’s): Clinical manifestations

A
  • Hyperpigmentation
  • Progressive weakness, severe chronic fatigue
  • Decreased GI function: Poor appetite, weight loss / difficulty maintaining weight
  • Chronic Hypotension
122
Q

What causes the hyperpigmentation in addison’s patients?

A

Excess ACTH on melanocytes

123
Q

Why do Addison’s patients experience chronic hypotension?

A

cortisol usually provides baseline tone to the vasculature; aldosterone helps maintain blood volume.
• Therefore, deficiencies lead to decreased tone, decreased blood volume.

124
Q

Blood levels in Addison’s (3)

A
  • Hyponatremia
  • Hyperkalemia
  • Hypoglacemic
125
Q

What is a severe complication of Adrenal Cortical Insufficiency?

A

In absence of adrenal cortex hormones, YOU CANNOT MOUNT AN ADEQUATE STRESS RESPONSE. Therefore, physical stress results in hypotension, shock, and risk of death.

126
Q

Cushing’s Syndrome: Cause (general)

A

Prolonged exposure to elevated levels of either endogenous glucocorticoids or exogenous glucocorticoids.

127
Q

Who is most susceptible to Cushing’s?

A

Women

128
Q

Cushing’s Syndrome: Cause (specific) - 4

A

o Exogenous steroid administration

o Endogenous glucocorticoid overproduction

o Primary adrenal lesions

o Ectopic ACTH production

129
Q

What patient would receive steroids? (3)

A
  • Patients with autoimmune disoders
  • Asthma
  • Transplant patients
130
Q

What would cause endogenous glucocorticoid overproduction?

A

ACTH-producing pituitary adenoma (rare)

131
Q

What would cause ectopic ACTH production? What in particular is implicated?

A
  • Tumors outside of pituitary gland

* Lung cancers particularly implicated

132
Q

Clinical manifestations of Cushing’s (11)

A

o Increases subcutaneous fat

o Decreases subcutaneous fat

o Face may be flushed

o Increases cognitive and emotional excitability

o Bone demineralization / bone breakdown

o Hyperglycemia

o Electrolyte imbalances

o Hypertensive

o Ovulatory dysfunction

o In females – excess facial hair

o Breakdown in skin integrity

133
Q

3 places a Cushing’s patient would experience increased fat:

A

Subcutaneously:
• In face (moon face)
• Between shoulder blades (buffalo hump)
• In middle of body (also nonsubq fat here)

134
Q

Electrolyte imbalances in a Cushing’s patient

A
  • Retention of sodium

* Loss of potassium

135
Q

Changes in vasculature with a Cushing’s patient

A
  • Vasoconstriction

* Left ventricular hypertrophy

136
Q

Changes in females with Cushing’s (2)

A
  • Amenorrhea

* Excess facial hair

Pathophys 2 (9 decks)

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