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endocrine Flashcards

1
Q

Endocrine System basic functions

A

Maintain metabolic equilibrium (homeostasis)
* Secrete chemical messengers (hormones)
* Regulate activity of various organs

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2
Q

how is the endocrine system regulated

A

feedback loops

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3
Q
  • Process of feedback inhibition
A
  • Increased activity of target tissue, typically down-regulates activity of gland secreting stimulating hormone**
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4
Q
  • Endocrine diseases
    a. hormone production?
    b. diseases associated with development of?
A

a. diseases of under/over-production of hormones
b. diseases associated with development of mass lesions

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5
Q

Classification of Endocrine Diseases

A
  • Too Little
  • Too Much
  • Other: Tumors
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6
Q

functional tumors

A

tumors of endocrine glands, whether benign or malignant, may secrete the hormone native to the gland. Such
tumors are said to be “functional” tumors. It may be the mass effect
of the tumor or the metabolic effect of the excessive hormone that
calls attention to the tumor.

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7
Q

Pituitary gland
where located?
connection?
role?
components?
how dx are divided?

A
  • Base of brain-sella turcica
  • Connected to hypothalamus
    a. stalk composed of axons
    b. venous plexus
  • Central role in regulation of other endocrine glands
  • Two components
    a. anterior lobe (adenohypophysis)
    b. posterior lobe (neurohypophysis)
  • Diseases divided according to lobe mainly affected
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8
Q

ant and post additonalt names

A

ant: adenohypophysis
post: neurohypophysis

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9
Q

what do the produce?

cells of the adenohypophysis

A

Somatotrophs: Produces growth hormone
* Lactotrophs: Produces prolactin
* Corticotrophs: Produces adrenocorticotrophic hormone
* Thyrotrophs: Produces thyroid simulating hormone
* Gonadotrophs: Produces follicle stimulating hormone and luteinizing
hormone

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10
Q

hormones of the neurohypophysis

A

ADH and oxytocin

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11
Q

dx of the ant pituitary

A

a. Decreased/increased secretion of trophic hormones
b. Hypopituitarism/hyperpituitarism

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12
Q

Hypopituitarism causes

A

a. Destructive lesions/processes –ischemia, radiation, inflammation, neoplasms

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13
Q

local effects of the cause?

Hyperpituitarism cause

A

Hyperpituitarism
a. Functional adenoma within anterior lobe
b. Local mass effects –enlargement of sella turcica, visual field abnormalities, increased intracranial pressure

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14
Q

Hypopituitarism can result from?

A
  • Pituitary Adenomas
  • Radiation Treatment
  • Neurosurgery
  • Sheehan Syndrome/ Ischemic necrosis of pituitary gland
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15
Q

growth? fertility? sex? lactation? thyroid? adrenal?

Clinical Manifestation:
Hypopituitarism

A
  • Pituitary Dwarfism
  • Amenorrhea & Infertility
  • Libido & Impotence
  • Postpartum lactation failure
  • Hypothyroidism
  • Hypoadrenalism
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16
Q

Hyperpituitarism can result from?

A
  • Pituitary Adenomas
  • Pituitary Hyperplasia
  • Pituitary Carcinomas
  • Hypothalamic disorders
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17
Q

Possible clinical Manifestations of Hyperpituitarism

A
  • Gigantism
  • Acromegaly
  • Cushing disease
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18
Q

usual cause? affects? when?

gigantism

A
  • Primary tumor causing Excess growth hormone (GH)- Adenoma of anterior pituitary
  • 2nd most common form
  • Affects all “growing tissues”
  • Gigantism- before growth
    plate closure
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19
Q

head? fatique? bones/joints? bp? heart?

gigantism signs

A

*Generalized overgrowth= 3 standard deviations
*Headaches
*Chronic fatigue
*Arthritis, osteoporosis
* Muscle weakness
*Hypertension
*Congestive heart failure

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20
Q

when is it diagnosed? vision? enlarged?

acromegaly

A
  • Late diagnosis, excess GH after plate closure
  • Poor vision; photophobia
  • Enlarged skull, hands, feet, ribs
  • Soft tissue, viscera
  • Enlarged maxilla, mandible, nasal and frontal bones, maxillary sinus
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21
Q
  • Intraoral signs of acromegaly
A
  • Diastemas
  • Malocclusion
  • Macroglossia
  • Enlarged lips
  • Sleep apnea
  • open bite
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22
Q
A

classic acromegaly

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23
Q

Posterior Pituitary dx

A
  • Diabetes Insipidus (Central)
  • Secretions of Inappropriately High
    Levels of ADH (SIADH)
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24
Q
  • Diabetes Insipidus (Central) signs
A
  • Polyuria
  • Dilute urine
  • Polydipsia
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25
Q

Na? cerebral? neruo? body water V? blood V? edema?

  • Secretions of Inappropriately High
    Levels of ADH (SIADH) signs
A
  • Hyponatremia
  • Cerebral edema
  • Neurologic dysfuction
  • increased Total Body Water
  • Blood volume normal
  • No peripheral edema
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26
Q

iodide of the thyroid

A

from diet
stored in the thyroid bound to thyroglobulin

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27
Q

thyroid hormones

A

T3 and T4, stored and produced in the thyroid

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28
Q

production of T3/4

A

T4 produced exclusively in the thyroid and majority of t3 is a result of T4 cleavge

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29
Q

how is T4/3 syn activated

A

stimulated by TSH released from the ant pit due to TRH from the hypothalamus
all this stiumlated with low T3/4

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30
Q

metabollically active forms of the hormones

A

only the non bound forms of thyroid horrmones are active

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31
Q

how is T3/4 syn shut off?

A

negative feedback with high levels of the hormones

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32
Q

BMR? carb metab? pro metab? lipid metab? thermogenesis? ANS?

hypothyroidism physio effects?

A
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33
Q

BMR? carb metab? pro metab? lipid metab? thermogenesis? ANS?

hyperthyroidism

A
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34
Q

primary Hypothyroidism causes

A
  • Intrinsic abnormality
    in the thyroid
  • Surgery
  • Radiotherapy
  • Autoimmune
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35
Q

secondary hypothyroidism due to

A

pituitary failure

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36
Q

types of hypothyroidism

A

myxedema and cretinism

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37
Q

when? signs? (energy? mental? cold? weight?)

myxedema

A
  • Adult onset hypothyroidism
  • Generalized fatigue
  • Apathy
  • Mental sluggishness
  • Listless
  • Cold intolerance
  • Overweight
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38
Q

age? skeleton? mental? face? teeth?

  • Cretinism
A
  • Childhood
  • Impaired skeletal development
  • Severe mental retardation
  • Short stature
  • Course facial features
  • Delayed tooth eruption
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39
Q

general signs of hypothyroidism

A
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40
Q

tongue with hypothyroid

A

macroglossia

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41
Q

hormone levels of hypothyroidism

A

high TSH/ TRH
Low T3/4
values retun to normal with tx

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42
Q

TSH levels of primary and secondary hypothyroid

A
  • Increased= Primary
  • Decreased= Secondary
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43
Q

tx hypothyroidism

A

supplementation

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44
Q

due to? enlargement of? risk of?

Hashimoto Thyroiditis

A
  • Autoimmune
  • Painless enlargement of thyroid: Symmetric & diffuse
  • Risk of B-cell non-Hodgkins Lymphomas
  • causes hypothyroidism
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45
Q

Large soft tissue lesion at midline in posterior of tongue?

A

refer to endocrinologist, could be thyroid tissue

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46
Q

neck? eyes? heat? weight? GI? heart? behavior?

Clinical signs and symptoms of hyperthyroidism

A

Goiter (small)
Exophtalmus (frequent)
Heat intolerance
Weight loss
Malabsorption and diarrhea
Tachycardia
Irritability and anxiety

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47
Q

common causes hyperthyroidism

A

Autoimmune - Graves’ disease

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48
Q

lab findings of hyperthyroidism

A

T4 and Free T4 elevated
T3 and Free T3 elevated
TSH and TRH suppressed

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49
Q

symptoms of hyperthyroidism

A
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50
Q

why is TSH/TRH low in hyper

A

T3/4 feedback inhibition

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51
Q

pathogenmic signs of the eyes for hyperthyroid

A

exopthalamy

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52
Q

Graves Disease s/s?

A
  • Tachycardia
  • Increased appetite
  • Weight loss
  • Exophthalmos
  • Intolerance to heat
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53
Q

how does graves dx come about?

A

auto Ab to the TSH receptor= increased stimulation and hyperthyroidism

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54
Q

tx of graves dx

A

ablation

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55
Q

caused by? signs? fatal?

potential severe event of graves dx

A
  • Thyroid storm
  • Caused by infection, stress,
    trauma
  • Elevated body temp.
  • Tachycardia
  • 20-40% mortality
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56
Q

can be due to?

Diffuse & Multinodular Goiter

A
  • Thyroid enlargement causing Impaired synthesis of thyroid hormone (NON-CANCEROUS)
  • can be due to: Iodine deficiency- (Endemic) OR Hyperplasia of follicles due to Pituitary stimulation
  • Maintenance of minimal function
    (euthyroid)
  • Diffuse early on, then nodular
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57
Q

Sequence Of Events In Endemic Goiter

A
  • Diet deficient in iodine
  • Decreased output of T3 & T4 by thyroid
  • Pituitary responds by secreting TSH
  • Thyroid hyperplasia
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58
Q
A

goiter

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59
Q

types of thyroid neoplasias

A

ademona
papillary carcinoma
follicular carcinoma
medullary carcinoma

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60
Q

number? malignant? sex? age? nodules?

thyroid adenoma

A
  • Solitary, BENIGN
  • Males
  • Younger
  • Warm/Cold nodules
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61
Q

% of neoplasias? ages? tx? worse in?

Papillary Carcinoma of thyroid

A
  • 75-85% of neplasias, MALIGNANT
  • All ages
  • Radiation
  • Worse in elderly
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62
Q

% neplasias? ages? due to? nodules?

  • Follicular Carcinoma of thyroid
A
  • 10-20%, MALIGNANT
  • Older
  • Iodine deficiency
  • Cold nodules
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63
Q

% neoplasias? cells/origin? inherited disorders? depositon of?

  • Medullary Carcinoma of thyroid
A
  • 5%, MALIGNANT
  • Neuroendocrine
  • Calcitonin (C cells)
  • Amyloid depostion in thyroid
  • MEN 2 A/B (20%)
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64
Q

metastisis to thyroid

A

possible due to other tissue malignancies

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65
Q

clasts? renal? vit D? secretion of? absorbtion of?

PTH functions

A

Activates osteoclasts activity
Increases Ca renal tubular resorption
Increases conversion of Vit. D into the active dihydroxy form in the kidneys
Increases urinary excretion of phosphates
Increases Ca absorption by the GI tract.

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66
Q

sugical? congenital? IS?

how can hypoPTH be induced

A

*Surgically induced=Iatrogenic
*Congenital absence = DiGeorge Syndrome
*Autoimmune= APECED

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67
Q

Ca? tentay? signs/tests?

signs of hypoPTH

A

*Hypocalcemia
*Tetany
*Chvostek Sign- Tapping CN VII causes Muscle contraction of Eye, mouth, nose
*Trosseau sign- Occluding circulation of forearm (BP cuff) causes Carpal spasm

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68
Q

effect of hypoPTH on teeth

A

enamel hypoplasia, can lead to pitting and chipping appearence

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69
Q

eruption of teeth with hypoPTH

A

delayed

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70
Q

possible pathologies of hyperPTH

A

primary and secondary

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71
Q

% each

primary hyperPTH causes

A
  • Adenoma (75-80%), One gland, benign
  • Hyperplasia (10-15%): Multiglandular and MEN 1 & 2a,b
  • Carcinoma (<5%), malignant
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72
Q

leads to?

secondary hyperPTH due to?

A
  • Renal failure: Hyperphosphatemia, Chronic hypocalcemia, Vitamin D deficient
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73
Q

skeleton? tumors formed? renal? what calcification can occur?

morphological changes with hyperPTH

A

Skeletal changes - bone resorption
- Formation of bone cysts and hemorrhages
(osteitis fibroso –cystica)
- Brown tumors
-Urinary tract stones (nephrolithiasis)
- Metastatic calcification: Serum calcium levels, especially Ionized calcium levels are high

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74
Q

Primary Hyperparathyroidism
ion levels and urinary excretion

A

Primary Hyperparathyroidism=Hypercalcemia and Hypophosphatemia
* Increased urinary excretion of both calcium and phosphate

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75
Q

SECONDARY HYPERPARATHYROIDISM due to?

A

Calcium is chronically depressed and low serum calcium levels lead to compensatory hyperactivity of the
parathyroids
Serum phosphate levels are elevated

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76
Q

renal? vitamin? dietary? stool?

causes of secondary hyperPTH

A

Chronic renal failure
Vitamin D deficiency
Inadequate dietary calcium
steatorrhea

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77
Q

PTGs? bones? calcification?

morpholgy changes seen with hyperPTH

A

Hyperplastic parathyroid glands
Bone chages (see primary hyperparathyroidism)
Metastatic calcification

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78
Q

renal osteodystrophy

A

a complication of chronic kidney disease that weakens your bones. It’s caused by changes in the levels of minerals and hormones (PTH) in your blood.
The main signs are bone pain and fractures. There’s no cure except for a kidney transplant.
seen with hyper PTH

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79
Q

severity? bone? blood vessels?

clinical features of secondary hyperPTH

A

Not as severe as in primary hyperparathyroidism
Related to symptoms secondary to chronic renal failure
Bone abnormalities (due to renal osteodystrophy)
Calciphylaxis (Ca in small blood vessel)
Tertiary hyperparathyroidism

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80
Q

bones? common tumor? kidneys? ulcers where? mental?

hyperPTH signs

A
  • Osteomalacia & loss of lamina dura
  • Brown tumor
  • Nephrolithiasis-kidney stones
  • Peptic/duodenal ulcers
  • Mental changes
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81
Q

Stones, Bones, Moans & Groans of hyperPTH

A
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82
Q

brown tumor of hyperPTH

A

resembles giant cell granuloma
would req a biopsy to distinguish
also req lab results to diagnose

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83
Q

palate in hyperPTH

A

palatal swelling

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84
Q

lamina dura with hyperPTH

A

lost

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85
Q

actions of PTH

A
  • Increases serum calcium
  • Activates osteoclasts
  • Increases renal tubular reabsorption of calcium
  • Increases renal conversion of Vit D
  • Increases urinary excretion of phosphate
  • Increased gastric absorption of calcium
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86
Q

layers of the adrenal gland

A

capsule
cortex
medulla

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87
Q

zones of the cortex

A

zona glomerulosa
zona fasiculata
zona reticularis

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88
Q
  • Zona Glomerulosa
    produces/reg by?
A
  • Aldosterone
  • Regulated by angiotensin II
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89
Q
  • Zona Fasiculata
    produces/reg by?
A
  • Glucocorticoids (cortisol)
  • Regulated by ACTH (biofeedback)
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90
Q
  • Zona Reticularis
    produces/ feedback?
A
  • Androgens
  • No feedback with ACTH
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91
Q

medulla produces?

A

Epi/ NE

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92
Q

acute? primary chronic?

Adrenal Cortex Pathology
Too Little:

A
  • Adrenal insufficiency
  • Acute: Waterhouse-Friderichsen
  • Primary Chronic: Addison Disease
  • Secondary
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93
Q

different forms

Adrenal Cortex Pathology
too much:

A
  • Hyperaldosterism
  • Hypercorticolism– Cushing Syndrome
  • Adrenogenital syndrome
94
Q

destruction of? IS? neoplasia? infections? secondary?

addisons dx causes

A
  • Destruction of adrenal cortex= decreased Production of adrenal corticosteroid hormones
  • Autoimmune
  • Metastatic carcinoma
  • Infections: TB/ Deep fungal
  • Secondary hypoadrenocorticism- Disorder of hypothalamus or pituitary gland (ACTH)
95
Q

appear when? fatique? bp? GI? pigment? acute crisis?

Addison’s Disease s/s

A
  • Clinical symptoms appear late
  • Weakness & Fatigue
  • Hypotension (postural)
  • GI disturbances
  • Hyper-pigmentation (Bronzing)
  • Adrenal Crisis (Acute)
96
Q

GI signs of addisons

A
  • Nausea/ Vomiting (N/V)
  • Anorexia
  • Diarrhea
  • Weight Loss
  • Salt cravings ( K+ ↑, Na+↓,)
97
Q

where can this be seen?

hyperpigmentation of addisons mechanism

A
  • ACTH precursor stimulates melanocytes
  • Frictional areas
  • can be seen orally on gingiva/ventral tongue
98
Q

results of adrenal crisis of addisons

A
  • Abdominal pain
  • Hypotension
  • Vascular collapse
99
Q
A

hyperpigmentation of addisons dx

100
Q

forms of hypercortisolism

A

primary and secondary

101
Q

what is excess? common demographic? causes and %?

primary hypercortisolism

A
  • Too much endogenous steroid
  • Females 5x in 3rd decade
  • Pituitary adenomas (ACTH), 50%= Cushing disease
  • Adrenal hyper/neoplasia,10-20%
  • Neuroendocrine tumors: Produce ACTH = Small Cell Lung Carcinoma
102
Q

common? due to?

exogenous steroids and hypercortisolism

A
  • Most common
  • Exogenous roids
  • Rule of 2s
  • Can become hypocortisol
    without taper
103
Q

pituitary cushing syndrome

104
Q

adrenal cushing syndrome

105
Q

paraneoplastic cushing syndrome

106
Q

iatrogenic cushing syndrome

A

occurs without taper

107
Q

cushing syndrome presentation

A
  • Central obesity
  • Peripheral wasting
  • Buffalo hump
  • “Moon facies”
  • Abdominal striae
  • Hirsutism
  • Poor wound healing
  • Diabetes
  • Hyperglycemia
  • Osteoporosis
  • Hypertension
108
Q

adrenal neoplasias of the cortex

A

adenomas and carcinomas

109
Q

adenomas of the cortex result in?

A
  • Cushing
  • Hyperaldosteronism
  • “Incidentalomas” possibly seen (incidentally found asymptomatic tumors)
110
Q

virilizing tumor

A

tumor of the cortex causing excess adrenal androgens

111
Q

Beckwith-
Wiedemann syndrome

A

inherited syndrome, causes overgrowth of the body (precancerous condition)

112
Q

Li-Fraumeni syndrome

A

inherited cancer risk due to TP53 mutation

113
Q

rarity?

predespositions to carcinomas of the cortex

A
  • Rare
  • Virilizing adenoma
  • Li-Fraumeni & Beckwith-
    Wiedemann
114
Q

arise from? % rule?

types of medulla neoplasias

A
  • Pheochromocytoma: arises from chromafiin cells
  • Neuroblastoma: arises from nn tissue
  • 10% tumor: 10% Familial (MEN 2A,B) ,10% extra-adrenal,10% are bilateral, 10% are malignant
115
Q

inheritance? chromo? gene affected?

Multiple Endocrine Neoplasias types

A
  • MEN 1- AD; Chr 11q (TSG)
  • MEN 2A- AD; Chr10q (RET proto-onco gene)
  • MEN 2B
116
Q

where they occur and name? incidence rate?

tumors of MEN 1AD

A
  • Pancreas (95%): insulinomas, gastrinomas
  • Parathyroid (40%): hyperplasia
  • Pituitary (30%): Prolactinomas
117
Q

where?

MEN 2A tumors

A
  • Adrenal Medulla (50%)
  • Med.Thyroid Carcinoma
  • PT- hyperplasia
118
Q

additional signs?

MEN 2B similarity to 2A

A
  • MEN 2A + marfanoid habitus; mucosal neuromas
119
Q

inheritence?

MEN 2B signs

A
  • AD
  • Marfanoid body type
  • Medullary thyroid carcinoma
  • Pheochromocytomas: Adrenal medulla
  • Neuromas
120
Q

neuromas of MEN2B

A
  • Can be first sign
  • Soft painless papules
  • Lips, conjunctiva, tongue,
    palate, buccal mucosa
  • Sentinel neuromas
121
Q
A

neuromas MEN2B

122
Q
A

neuromas MEN2B

123
Q

what tissue is seen in a neuroma

124
Q

McCune-Albright
Syndrome

A

irregular bordered pigmentation
fibrous dysplasia may occur

125
Q

portions of the pancreas

A

exocrine and endocrine

126
Q

dx of this?

  • Exocrine Pancreas
A
  • Exocrine Pancreas
  • Secretes enzymes for Digestion= Inactive proenzymes

dx include:
Acute pancreatitis
Chronic pancreatitis
Cancer

127
Q
  • Endocrine Pancreas
A
  • Secretes hormones for Glucose homeostasis and Other metabolic activities
  • Diabetes mellitus, Beta cells in the islets of Langerhans
128
Q

injury to? possible forms? results?

Acute Pancreatitis due to:

A
  • Injury to acinar cells
  • Interstitial or edematous pancreatitis: Mild and Reversible
  • Acute hemorrhagic pancreatitis due to Alcoholism or Chronic biliary disease (often fatal)
129
Q

Acute Pancreatitis Etiology
metabolic?
alc?
hyper?
drugs?
genes?

A
  • Metabolic
  • Alcoholism
  • Hyperlipoproteineimia
  • Hypercalcemia
  • Drugs: Thiazide diuretics
  • Genetic
130
Q

mechanical factors of acute pancreatitis

A
  • Trauma
  • Gallstones
  • Iatrogenic injury: Perioperative injury
    or Endoscopic procedures with dye injections
131
Q

vascular causes of acute pancreatitis

A
  • Shock
  • Atheroembolism
  • Polyarteritis nodosa
132
Q

infections that can cause acute pancreatitis

A
  • Mumps
  • Cocksackievirus
  • Mycoplasma pneumoniae
133
Q

Chronic Pancreatitis causes
destruction of?
intermittent attacks?
alc?
pancreatic duct? how?
acinar cells?

A
  • Destruction of pancreatic parenchyma
  • Intermittent “acute” attacks
  • Alcoholism
  • Obstruction of pancreatic duct due to:
    Mechanical blockage
    Congenital defects
    Cancer
    Inspissated mucous
  • Chronic injury to acinar cells
134
Q

possible Exocrine Pancreatic
Neoplasms

A
  • Pancreatic cystic neoplasm
  • Pancreatic cancer
  • Acinar cell carcinoma
135
Q

possible Endocrine Pancreatic
Neoplasms

A
  • Islet cell tumors
  • Pancreatic Gastrinoma
136
Q

names? present with?

  • Islet cell tumors
A
  • Insulinoma (excess insulin)
  • Glucagonoma: presents with Mild diabetes and Rash
137
Q

name? causes what effects?

  • Pancreatic Gastrinoma
A
  • Zollinger-Ellison Syndrome
    causes:
  • Hypersecretion of gastric acid
  • Peptic ulcers
  • High blood gastrin
138
Q

portion of the pancreas concerned with diabetes

A

Endocrine Pancreas
* Islets of Langerhans
* Alpha cells –glucagon
* Beta cells –insulin - diabetes mellitus

139
Q

effects on mm, fat, liver?

insulin physiology

140
Q

Diabetes Mellitus
* glycemia?
* types?
* result?

A

Diabetes Mellitus
* Hyperglycemia
* Lack of insulin (Type 1)
* Resistance to insulin (Type 2)
* Combination
* Loss of insulin (anabolic) results in a catabolic state affecting glucose, fat & protein metabolism

141
Q

Type 1 Diabetes Mellitus

A

Archaic terminology: Insulin Dependent DM, juvenile-onset DM
* Autoimmune destruction of B cells in the Islets of Langerhans (insulitis)
* Absolute deficiency of insulin
* Only 10% diabetics
* Avg. age of onset- 14 yo

142
Q

acute/chronic

emergenices of type 1

A
  • Acute: hypoglycemia
  • Chronic: ketoacidosis
143
Q

potential causes of type 1

A
  • Destruction of β-cells due to:
  • Autoimmune
  • T cell mediated
  • Auto-antibodies
  • Genetic
  • 30-70% twin concordance
  • HLA-DR3, DR4 (90-95%)
  • Environmental? (Infectious)
144
Q

diagnosis of both type 1 and 2

A
  • WNL= 70-120 mg/dL
  • Any of these
  • ≥ 200 mg/dL + S/S
  • Fasting ≥ 126 mg/dL
  • OGTT ≥ 200 mg/dl (2 hrs)
145
Q

what can be potential causes/interact to caused Type 1
Diabetes Mellitus

A
  • Genetic factors
  • Autoimmunity
  • Environmental factors: Viruses
    (Coxsackie B) and Chemicals
146
Q

Diagnosis of
Diabetes Mellitus

A
  • Fasting venous plasma glucose of >140 mg/dl on more than
    one occasion
  • Following ingestion of 75 grams of glucose
  • 2hr venous plasma glucose concentration >200 mg/dl
  • At least one glucose value during that period is >200 mg/dl
147
Q

Diabetes Mellitus Type 2

A
  • Adult onset
  • “Relative” lack of insulin
  • 80-90% of diabetics
  • Insulin resistance
  • Early Normal blood insulin level
  • Target tissue Resistance
  • β-cell dysfunction fails to
    compensate
148
Q

demographics of type 2

149
Q

emergency associated with type 2

A
  • Ketoacidosis (rare) which can lead to Coma due to hyperosmolarity
150
Q

old term for type 2

A

Non-Insulin dependent DM, adult/maturity-onset DM

151
Q

type 2 can be due to

A

Inadequate secretion of insulin from the pancreas
* Reduced tissue sensitivity to insulin (liver, skeletal muscle, adipose tissue)
* Initially, hyperinsulinemia may compensate for peripheral insulin resistance and normal plasma glucose is maintained
* Eventually, B cell compensation becomes inadequate and there is progression to hyperglycemia

152
Q

risk factors of type 2

A

*Obesity
*Genetics
*50-90% of twins
*20-40% of 1st degree
* Only 5-7% in populatio

153
Q

clinical pres? HLA family history twins? pahtogenesis? islet cells

type 1/2 comparison chart

154
Q

ketosis of DM

A
  • Ketosis (chronic): Ketone bodies (alternative energy source), can lead to Ketoacidosis & diabetic coma= DM1
    or Hyperosmolar non-ketotic coma= DM2
155
Q

Clinical Progression of DM

A

Only after 90% destruction of the 10^6 β-cells
* Polyuria
* Polydypsia
* Polyphagia
* Fatigue/wasting

156
Q

values?

HbA1c

A

The fraction of glycosylated hemoglobin in circulating red blood cells
* Reflects the degree of hyperglycemia
during the preceding 6-8 weeks
<6%; good
8.0%; caution
>9%; action suggested

157
Q

vascular dx’s of DM

A
  • Macrovascular disease –large and medium-sized arteries
  • Microvascular disease –capillary dysfunction in target organs
158
Q

Macrovascular Disease of DM

A

Accelerated Atherosclerosis
* Heart - myocardial infarction
* Brain - stroke
* Peripheral vascular disease –lower extremity gangrene

159
Q

Microvascular Disease of DM

A

Diabetic Microangiopathy
* Retina –diabetic retinopathy
* Kidneys –nephropathy
* Peripheral nerves - neuropathy

160
Q

late complications of DM variabilty

A

Great variability among patients in:
* Time of onset
* Severity
* Organs involved

161
Q

what can delay onset of DM complications

A

Tight glycemic control delays onset

162
Q

late DM complcations most likely to be seen in what tisses?

A
  • Arteries (macrovascular changes)
  • Basement membrane of small vessels (microangiopathy)
  • Kidneys (diabetic nephropathy)
  • Retina (diabetic retinopathy)
  • Nerves (diabetic neuropathy)
163
Q

most common cause of death in DM

164
Q

seen with what dx? result of this?

hyaline artiolosclerosis seen where?

A

seen with DM
* * Kidneys
* Leads to Hypertension

165
Q

microangiopathy of DM

A
  • Thickened Basement membranes (but still leaky)
  • Nephropathy, Retinopathy, Neuropathy,
166
Q

Acanthosis Nigricans

A
  • A dermatosis characterized by velvety, papillomatous, brownish-black,
    hyperkeratotic plaques, typically of the
    intertriginous surfaces and neck
  • May be associated with insulin resistance (cutaneous marker for type 2 diabetes)
  • May be associated with internal malignancy
167
Q

seen with? can indicate?

A

Acanthosis Nigricans, seen with obesity and diabetes
can indicate internal malignancy

168
Q

infections? healing? gingiva? xero? parotid?

oral complications of DM

169
Q
A

mucomycosis (zygomycosis)

170
Q

change in fucntion? key to this?

liver regen capacity?

A
  • Regenerative
  • CanRemove 60%
  • Minimal change in function
  • 4-6 weeks for almost total
    regeneration of mass
  • The key is the hepatic reticulum= Type 4 collagen with Fibrosis= Types 1 & 3 collagen
171
Q

functions of liver

A

metabolic
syn plasma pro
storage
degrade/detox
exocrine
endocrine

172
Q

metabolic liver function

A

glucose homeostasis

173
Q

plasma pro made by liver

A

Albumin, VLDL, LDL, PT,
Fibrinogen

174
Q

what can be stored in liver

A
  • Glycogen
  • Triglycerides
  • Iron, Copper
  • Vitamins- A, D, K
175
Q

phases?

detox function of liver

176
Q

exocrine function of liver

177
Q

endocrine fucntions of liver

A
  • D3 to 25-hydroxy-cholecalciferol
  • T4 to T3 (active)
  • GHRH
  • Insulin & glucagon degradation
178
Q

what chemical? infection? dx? Fe? IS? idiopathic?

Causes of Cirrhosis

A
  • ETOH (alc)
  • Infection (HBV, HCV)
  • Biliary disease
  • Iron overload (Hemochromatosis)
  • Autoimmune hepatitis
  • 10% idiopathic
179
Q

how tissue is effected

Cirrhosis Characteristics

A
  • Diffuse fibrosis and conversion of normal architecture into abnormal nodules
  • Bridging fibrosis
  • Parenchymal nodules: Micro (3mm);Macro, regeneration
  • Entire liver architecture effaced
180
Q

Complications of Cirrhosis

A
  • LOF
  • Portal hypertension
  • Hepatocellular Carcinoma
181
Q

cells lost? blood dynamics?

LOF with cirrhiosis

A
  • Hepatocyte death= Loss of Microvilli
  • Changes in blood flow with decreased Proteins
182
Q

mechanism/leads to?

portal hypertension

A
  • Loss of Type 4 collagen
  • Loss of fenestrated sinusoids= Low to high pressure
  • Pressure on central veins due to fibrosis
  • leads to: Ascites, Portosystemic venous shunts= Varices, and Splenomegaly
183
Q

physical appearence? venous adaption? spleen? NS?

Portal Hypertension
Clinical Consequences

A
  • Ascites
  • Formation of portosystemic venous shunts (liver bypassed)
  • Congestive splenomegaly
  • Hepatic encephalopathy (build up of toxins in blood alters NS function)
184
Q

type of fluid?

Complications of Cirrhosis: Ascities

A
  • Fluid in the peritoneum (500mL)
  • Serous fluid
185
Q

what can enhance this?

pathogenesis of ascites

A
  • Alteration of Starling Forces in the
    sinusoids
  • Fluid is forced into Space of Disse
  • Enhanced by hyoalbuminemia
  • Enhanced hepatic lymphatic drainage
  • Overwhelms capacity of thoracic duct
    drainage
186
Q

skin? albumin? NH? glucose? estrogen? coagulation?

s/s of liver failuire

187
Q

dx? possible causes? what are the possible indications of each cause?

juandice

A

Jaundice is not a disease
* NON-SPECIFIC sign of liver dysfunction
* Retention of bile (>2.0 mg/dL) due to:
1. Hepatitis
1. Obstruction (cirrhosis)=Accumulation of conjugated bilirubin
1. Hemolytic anemias=Accumulation of un-conjugated bilirubin
1. Cholestasis (Lack of flow of bile) due to Retention due to obstruction or hepatocyte dysfunction, Serum Alk Phos elevated

188
Q

Icterus

A

yellowing of eyes w juandice

189
Q

where can juandice be seen orally

190
Q

Causes of Liver Disease

A
  • Alcohol related
  • Drug related
  • Infectious (HCV)
  • Metabolic
  • Neoplasms
  • Autoimmune
191
Q

types of dx? %chronic liver dx from OH? % deaths due to OH?

Alcoholic Liver Disease

A
  • ETOH causes 60% of Chronic Liver Disease
  • ETOH accounts for 40-50% of deaths due to cirrhosis
  • Forms of liver disease:
    1. Hepatitic steatosis (fatty liver)
    1. Alcoholic hepatitis
    1. Cirrhossis
192
Q

forms of Drug-induced Liver Disease

A
  • Predictable(intrinsic)
  • Unpredictable(idiosyncratic)
  • Toxicity + immune reaction
193
Q

tetracycline affect at liver

A

microvascular fatty liver

194
Q

antineoplastic drugs effect at liver

A

macrovascular fatty change with chriosis and fibrosis

195
Q

amanita phalloides (mushroom toxin) effect at liver

A

diffuse/massive necrosis

196
Q

CCl4 at liver

A

centrilobular necrosis

197
Q

ETOH affect at liver

A

macrovascular change
fibrosis and chriosis

198
Q

can we distinguish drug induced liver dx

A
  • Drug induced chronic hepatitis is
    indistinguishable from other causes:
    1. Alcoholic liver disease
    1. Viral Hepatitis
  • Need serology to r/o viral
199
Q

types of hep

200
Q

transmissions of the dif hep

201
Q

HepA
* limiting?
* carrier state?
* immunity?
* Vaccine?
* Epidemics?
* fatalities?

A
  • Self limiting
  • No carrier state
  • Life long immunity
  • Vaccine
  • Epidemics
  • Rare fatalities (0.1%)
202
Q

incubation? carrier? increased risk for? vax?

HepB

A
  • Prolonged incubation
  • Chronic carrier state
  • Increased risk of HCCa
  • Vaccine- Anti-HBs
203
Q

similar to? risk? related to?

HCV

A
  • Similar to HBV, but…
  • More cirrhosis risk
  • Used to be transfusion
    related
  • IV drug related
  • Early Tx hopeful for cure
204
Q

needs? chance?

HDV

A
  • Needs HBV (HBsAg)
  • Coinfection of B & D at same time
  • low chance
  • Super-infection of a carrier of HBV that gets a new HDV
  • More likely
205
Q

WNL? demographics? deposits where?

Hemochromatosis

A
  • Excessive accumulation of Iron
  • WNL= 2-6 gms (only 0.5gm in liver)
  • Males 5-7:1 ( earlier than females)
  • 5th-6th decades
  • Iron deposition in liver, pancreas, myocardium,
    skin, joints
206
Q

types of hemochromatosis

A
  • Hereditary hemochromatosis
  • Acquired hemochromatosis
207
Q

inheritence? gene/chr? what is lost? net gain?

  • Hereditary hemochromatosis
A
  • AR most common
  • HFE gene on Chr 6p
  • Regulation of intestinal absorption is lost
  • Net gain/year of 0.5-1.0 gm
208
Q

associated patholgy?

  • Acquired hemochromatosis
A
  • Known source of excess iron
  • Hemolytic anemia associated with ineffective erythropoiesis
209
Q

liver? skin? pancreas?

Hemochromatosis can present with?

A
  • Hepatomegaly/dysfunction/Cirrhosis
  • Pancreatic fibrosis which can lead to DM
  • Skin pigmentation
210
Q

wilson dx genetics

A

mutation at chr 13

211
Q

wilsn dx is a disorder of?

A

copper metabolism

212
Q

where does copper accumulate with wilsons dx

A

liver, brain, eye

213
Q

what is the effect of wilson dx

A

normal copper uptake, but failure to enter circulation as ceruloplasmin
inability to be excreted int bile
spills into circulation unbund causing hemolysis

214
Q

age of onset? copper levels? liver? nn?

diagnosis of wilson

A
  • Onset prior to age 6
  • Elevated hepatic copper, low serum ceruloplasmin, high urinary copper
  • Acute/Chronic hepatitis
  • Neuropsychiatric
215
Q

neuro changes of wilson

A
  • Behavioral changes
  • Parkinson-like
  • Pychosis
  • Kayser-Fleischer rings
216
Q

demo? associated with? begins as? signs? mito? drugs associated?

reye syndrome

A
  • Fatty liver changes & encephalopathy in Kids (<4 yo)
  • Associated with viral infection recovery
  • Begins as pernicious vomiting 3-5 days s/p virus
  • Lethargy, irritability, hepatomegaly
  • Mitochondrial hepatopathy (LOF)
  • Aspirin association?
217
Q

neoplasias of liver can be

A

benign or malignant

218
Q

benign neoplasias of the liver

219
Q

most common malignancy? preceeding factor?

malignant neoplasias of the liver

220
Q

geographics/demographics? associated pathologies?

Hepatocellular Carcinoma
(Hepatoma)

A
  • Asia, Africa- 20-40 yo
  • 50% w/o cirrhosis
    • West much lower (8-30x less)
  • Seldom before 60 yo
  • 90% w/ cirrhosis
  • Cirrhosis (alcoholic)
  • HBV (200x), HCV
  • Aflatoxin (Aspergillus flavus)
221
Q

gallbladder functions

A
  • Stores bile
  • 50mL
  • Releases bile
  • Fat digestion
222
Q

gallbladder lacks ?

A

muscularis mucosae

223
Q

dx of gallbladder

A
  • Cholelithiasis
  • Cholecystitis
  • Tumors
224
Q

Cholelithiasis possible stones

A
  • Cholesterol stones: Crystalline cholesterol monohydrate
  • Pigment stones: Bilirubin Calcium salts
225
Q

Pathogenesis of Cholesterol Stones at gallbladder

A
  • Supersaturated bile with cholesterol
  • Gallbladder hypomotility
  • Accelerated cholesterol nucleation
  • Crystals trapped by gallbladder mucous hypersecretions
226
Q

Pathogenesis of Pigment Stones

A
  • Mixture of abnormal insoluble calcium salts of unconjugated
    bilirubin and inorganic calcium salts
227
Q

Cholecystitis forms

A

acute and chronic

228
Q

due to? are gallstones oresent?

acute cholecystits

A
  • Acute inflammation
  • Obstruction of the neck or cystic duct
  • Absence of gallstones
229
Q

due to? absecnce of? what forms?

chronic cholecystits

A

Sequel to repeated bouts of acute cholecystitis
* Absence of acute cholecystitis
* Gallstones

230
Q

possible tumors of gallbladder?

A
  • Carcinoma of the gallbladder
  • Carcinoma of the extrahepatic bile ducts

Pathology (20 decks)

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