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endocrine Flashcards

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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
# Na? cerebral? neruo? body water V? blood V? edema? * Secretions of Inappropriately High Levels of ADH (SIADH) signs
* Hyponatremia * Cerebral edema * Neurologic dysfuction * increased Total Body Water * Blood volume normal * No peripheral edema
26
iodide of the thyroid
from diet stored in the thyroid bound to thyroglobulin
27
thyroid hormones
T3 and T4, stored and produced in the thyroid
28
production of T3/4
T4 produced exclusively in the thyroid and majority of t3 is a result of T4 cleavge
29
how is T4/3 syn activated
stimulated by TSH released from the ant pit due to TRH from the hypothalamus all this stiumlated with low T3/4
30
metabollically active forms of the hormones
only the non bound forms of thyroid horrmones are active
31
how is T3/4 syn shut off?
negative feedback with high levels of the hormones
32
# BMR? carb metab? pro metab? lipid metab? thermogenesis? ANS? hypothyroidism physio effects?
33
# BMR? carb metab? pro metab? lipid metab? thermogenesis? ANS? hyperthyroidism
34
primary Hypothyroidism causes
* Intrinsic abnormality in the thyroid * Surgery * Radiotherapy * Autoimmune
35
secondary hypothyroidism due to
pituitary failure
36
types of hypothyroidism
myxedema and cretinism
37
# when? signs? (energy? mental? cold? weight?) myxedema
* Adult onset hypothyroidism * Generalized fatigue * Apathy * Mental sluggishness * Listless * Cold intolerance * Overweight
38
# age? skeleton? mental? face? teeth? * Cretinism
* Childhood * Impaired skeletal development * Severe mental retardation * Short stature * Course facial features * Delayed tooth eruption
39
general signs of hypothyroidism
40
tongue with hypothyroid
macroglossia
41
hormone levels of hypothyroidism
high TSH/ TRH Low T3/4 values retun to normal with tx
42
TSH levels of primary and secondary hypothyroid
* Increased= Primary * Decreased= Secondary
43
tx hypothyroidism
supplementation
44
# due to? enlargement of? risk of? Hashimoto Thyroiditis
* Autoimmune * Painless enlargement of thyroid: Symmetric & diffuse * Risk of B-cell non-Hodgkins Lymphomas * causes hypothyroidism
45
Large soft tissue lesion at midline in posterior of tongue?
refer to endocrinologist, could be thyroid tissue
46
# neck? eyes? heat? weight? GI? heart? behavior? Clinical signs and symptoms of hyperthyroidism
Goiter (small) Exophtalmus (frequent) Heat intolerance Weight loss Malabsorption and diarrhea Tachycardia Irritability and anxiety
47
common causes hyperthyroidism
Autoimmune - Graves’ disease
48
lab findings of hyperthyroidism
T4 and Free T4 elevated T3 and Free T3 elevated TSH and TRH suppressed
49
symptoms of hyperthyroidism
50
why is TSH/TRH low in hyper
T3/4 feedback inhibition
51
pathogenmic signs of the eyes for hyperthyroid
exopthalamy
52
Graves Disease s/s?
* Tachycardia * Increased appetite * Weight loss * Exophthalmos * Intolerance to heat
53
how does graves dx come about?
auto Ab to the TSH receptor= increased stimulation and hyperthyroidism
54
tx of graves dx
ablation
55
# caused by? signs? fatal? potential severe event of graves dx
* Thyroid storm * Caused by infection, stress, trauma * Elevated body temp. * Tachycardia * 20-40% mortality
56
# can be due to? Diffuse & Multinodular Goiter
* 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
57
Sequence Of Events In Endemic Goiter
* Diet deficient in iodine * Decreased output of T3 & T4 by thyroid * Pituitary responds by secreting TSH * Thyroid hyperplasia
58
goiter
59
types of thyroid neoplasias
ademona papillary carcinoma follicular carcinoma medullary carcinoma
60
# number? malignant? sex? age? nodules? thyroid adenoma
* Solitary, BENIGN * Males * Younger * Warm/Cold nodules
61
# % of neoplasias? ages? tx? worse in? Papillary Carcinoma of thyroid
* 75-85% of neplasias, MALIGNANT * All ages * Radiation * Worse in elderly
62
# % neplasias? ages? due to? nodules? * Follicular Carcinoma of thyroid
* 10-20%, MALIGNANT * Older * Iodine deficiency * Cold nodules
63
# % neoplasias? cells/origin? inherited disorders? depositon of? * Medullary Carcinoma of thyroid
* 5%, MALIGNANT * Neuroendocrine * Calcitonin (C cells) * Amyloid depostion in thyroid * MEN 2 A/B (20%)
64
metastisis to thyroid
possible due to other tissue malignancies
65
# clasts? renal? vit D? secretion of? absorbtion of? PTH functions
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.
66
# sugical? congenital? IS? how can hypoPTH be induced
*Surgically induced=Iatrogenic *Congenital absence = DiGeorge Syndrome *Autoimmune= APECED
67
# Ca? tentay? signs/tests? signs of hypoPTH
*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
68
effect of hypoPTH on teeth
enamel hypoplasia, can lead to pitting and chipping appearence
69
eruption of teeth with hypoPTH
delayed
70
possible pathologies of hyperPTH
primary and secondary
71
# % each primary hyperPTH causes
* Adenoma (75-80%), One gland, benign * Hyperplasia (10-15%): Multiglandular and MEN 1 & 2a,b * Carcinoma (<5%), malignant
72
# leads to? secondary hyperPTH due to?
* Renal failure: Hyperphosphatemia, Chronic hypocalcemia, Vitamin D deficient
73
# skeleton? tumors formed? renal? what calcification can occur? morphological changes with hyperPTH
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
74
Primary Hyperparathyroidism ion levels and urinary excretion
Primary Hyperparathyroidism=Hypercalcemia and Hypophosphatemia * Increased urinary excretion of both calcium and phosphate
75
SECONDARY HYPERPARATHYROIDISM due to?
Calcium is chronically depressed and low serum calcium levels lead to compensatory hyperactivity of the parathyroids Serum phosphate levels are elevated
76
# renal? vitamin? dietary? stool? causes of secondary hyperPTH
Chronic renal failure Vitamin D deficiency Inadequate dietary calcium steatorrhea
77
# PTGs? bones? calcification? morpholgy changes seen with hyperPTH
Hyperplastic parathyroid glands Bone chages (see primary hyperparathyroidism) Metastatic calcification
78
renal osteodystrophy
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
79
# severity? bone? blood vessels? clinical features of secondary hyperPTH
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
80
# bones? common tumor? kidneys? ulcers where? mental? hyperPTH signs
* Osteomalacia & loss of lamina dura * Brown tumor * Nephrolithiasis-kidney stones * Peptic/duodenal ulcers * Mental changes
81
Stones, Bones, Moans & Groans of hyperPTH
82
brown tumor of hyperPTH
resembles giant cell granuloma would req a biopsy to distinguish also req lab results to diagnose
83
palate in hyperPTH
palatal swelling
84
lamina dura with hyperPTH
lost
85
actions of PTH
* 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
86
layers of the adrenal gland
capsule cortex medulla
87
zones of the cortex
zona glomerulosa zona fasiculata zona reticularis
88
* Zona Glomerulosa produces/reg by?
* Aldosterone * Regulated by angiotensin II
89
* Zona Fasiculata produces/reg by?
* Glucocorticoids (cortisol) * Regulated by ACTH (biofeedback)
90
* Zona Reticularis produces/ feedback?
* Androgens * No feedback with ACTH
91
medulla produces?
Epi/ NE
92
# acute? primary chronic? Adrenal Cortex Pathology Too Little:
* Adrenal insufficiency * Acute: Waterhouse-Friderichsen * Primary Chronic: Addison Disease * Secondary
93
# different forms Adrenal Cortex Pathology too much:
* Hyperaldosterism * Hypercorticolism– Cushing Syndrome * Adrenogenital syndrome
94
# destruction of? IS? neoplasia? infections? secondary? addisons dx causes
* 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
# appear when? fatique? bp? GI? pigment? acute crisis? Addison’s Disease s/s
* Clinical symptoms appear late * Weakness & Fatigue * Hypotension (postural) * GI disturbances * Hyper-pigmentation (Bronzing) * Adrenal Crisis (Acute)
96
GI signs of addisons
* Nausea/ Vomiting (N/V) * Anorexia * Diarrhea * Weight Loss * Salt cravings ( K+ ↑, Na+↓,)
97
# where can this be seen? hyperpigmentation of addisons mechanism
* ACTH precursor stimulates melanocytes * Frictional areas * can be seen orally on gingiva/ventral tongue
98
results of adrenal crisis of addisons
* Abdominal pain * Hypotension * Vascular collapse
99
hyperpigmentation of addisons dx
100
forms of hypercortisolism
primary and secondary
101
# what is excess? common demographic? causes and %? primary hypercortisolism
* 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
# common? due to? exogenous steroids and hypercortisolism
* Most common * Exogenous roids * Rule of 2s * Can become hypocortisol without taper
103
pituitary cushing syndrome
104
adrenal cushing syndrome
105
paraneoplastic cushing syndrome
106
iatrogenic cushing syndrome
occurs without taper
107
cushing syndrome presentation
* Central obesity * Peripheral wasting * Buffalo hump * “Moon facies” * Abdominal striae * Hirsutism * Poor wound healing * Diabetes * Hyperglycemia * Osteoporosis * Hypertension
108
adrenal neoplasias of the cortex
adenomas and carcinomas
109
adenomas of the cortex result in?
* Cushing * Hyperaldosteronism * “Incidentalomas” possibly seen (incidentally found asymptomatic tumors)
110
virilizing tumor
tumor of the cortex causing excess adrenal androgens
111
Beckwith- Wiedemann syndrome
inherited syndrome, causes overgrowth of the body (precancerous condition)
112
Li-Fraumeni syndrome
inherited cancer risk due to TP53 mutation
113
# rarity? predespositions to carcinomas of the cortex
* Rare * Virilizing adenoma * Li-Fraumeni & Beckwith- Wiedemann
114
# arise from? % rule? types of medulla neoplasias
* 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
# inheritance? chromo? gene affected? Multiple Endocrine Neoplasias types
* MEN 1- AD; Chr 11q (TSG) * MEN 2A- AD; Chr10q (RET proto-onco gene) * MEN 2B
116
# where they occur and name? incidence rate? tumors of MEN 1AD
* Pancreas (95%): insulinomas, gastrinomas * Parathyroid (40%): hyperplasia * Pituitary (30%): Prolactinomas
117
# where? MEN 2A tumors
* Adrenal Medulla (50%) * Med.Thyroid Carcinoma * PT- hyperplasia
118
# additional signs? MEN 2B similarity to 2A
* MEN 2A + marfanoid habitus; mucosal neuromas
119
# inheritence? MEN 2B signs
* AD * Marfanoid body type * Medullary thyroid carcinoma * Pheochromocytomas: Adrenal medulla * Neuromas
120
neuromas of MEN2B
* Can be first sign * Soft painless papules * Lips, conjunctiva, tongue, palate, buccal mucosa * Sentinel neuromas
121
neuromas MEN2B
122
neuromas MEN2B
123
what tissue is seen in a neuroma
nn tissue
124
McCune-Albright Syndrome
irregular bordered pigmentation fibrous dysplasia may occur
125
portions of the pancreas
exocrine and endocrine
126
# dx of this? * Exocrine Pancreas
* Exocrine Pancreas * Secretes enzymes for Digestion= Inactive proenzymes dx include: Acute pancreatitis Chronic pancreatitis Cancer
127
* Endocrine Pancreas
* Secretes hormones for Glucose homeostasis and Other metabolic activities * Diabetes mellitus, Beta cells in the islets of Langerhans
128
# injury to? possible forms? results? Acute Pancreatitis due to:
* Injury to acinar cells * Interstitial or edematous pancreatitis: Mild and Reversible * Acute hemorrhagic pancreatitis due to Alcoholism or Chronic biliary disease (often fatal)
129
Acute Pancreatitis Etiology metabolic? alc? hyper? drugs? genes?
* Metabolic * Alcoholism * Hyperlipoproteineimia * Hypercalcemia * Drugs: Thiazide diuretics * Genetic
130
mechanical factors of acute pancreatitis
* Trauma * Gallstones * Iatrogenic injury: Perioperative injury or Endoscopic procedures with dye injections
131
vascular causes of acute pancreatitis
* Shock * Atheroembolism * Polyarteritis nodosa
132
infections that can cause acute pancreatitis
* Mumps * Cocksackievirus * Mycoplasma pneumoniae
133
Chronic Pancreatitis causes destruction of? intermittent attacks? alc? pancreatic duct? how? acinar cells?
* 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
possible Exocrine Pancreatic Neoplasms
* Pancreatic cystic neoplasm * Pancreatic cancer * Acinar cell carcinoma
135
possible Endocrine Pancreatic Neoplasms
* Islet cell tumors * Pancreatic Gastrinoma
136
# names? present with? * Islet cell tumors
* Insulinoma (excess insulin) * Glucagonoma: presents with Mild diabetes and Rash
137
# name? causes what effects? * Pancreatic Gastrinoma
* Zollinger-Ellison Syndrome causes: * Hypersecretion of gastric acid * Peptic ulcers * High blood gastrin
138
portion of the pancreas concerned with diabetes
Endocrine Pancreas * Islets of Langerhans * Alpha cells –glucagon * Beta cells –insulin - diabetes mellitus
139
# effects on mm, fat, liver? insulin physiology
140
Diabetes Mellitus * glycemia? * types? * result?
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
Type 1 Diabetes Mellitus
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
# acute/chronic emergenices of type 1
* Acute: hypoglycemia * Chronic: ketoacidosis
143
potential causes of type 1
* 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
diagnosis of both type 1 and 2
* WNL= 70-120 mg/dL * Any of these * ≥ 200 mg/dL + S/S * Fasting ≥ 126 mg/dL * OGTT ≥ 200 mg/dl (2 hrs)
145
what can be potential causes/interact to caused Type 1 Diabetes Mellitus
* Genetic factors * Autoimmunity * Environmental factors: Viruses (Coxsackie B) and Chemicals
146
Diagnosis of Diabetes Mellitus
* 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
Diabetes Mellitus Type 2
* 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
demographics of type 2
changing
149
emergency associated with type 2
* Ketoacidosis (rare) which can lead to Coma due to hyperosmolarity
150
old term for type 2
Non-Insulin dependent DM, adult/maturity-onset DM
151
type 2 can be due to
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
risk factors of type 2
*Obesity *Genetics *50-90% of twins *20-40% of 1st degree * Only 5-7% in populatio
153
# clinical pres? HLA family history twins? pahtogenesis? islet cells type 1/2 comparison chart
154
ketosis of DM
* Ketosis (chronic): Ketone bodies (alternative energy source), can lead to Ketoacidosis & diabetic coma= DM1 or Hyperosmolar non-ketotic coma= DM2
155
Clinical Progression of DM
Only after 90% destruction of the 10^6 β-cells * Polyuria * Polydypsia * Polyphagia * Fatigue/wasting
156
# values? HbA1c
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
vascular dx's of DM
* Macrovascular disease –large and medium-sized arteries * Microvascular disease –capillary dysfunction in target organs
158
Macrovascular Disease of DM
Accelerated Atherosclerosis * Heart - myocardial infarction * Brain - stroke * Peripheral vascular disease –lower extremity gangrene
159
Microvascular Disease of DM
Diabetic Microangiopathy * Retina –diabetic retinopathy * Kidneys –nephropathy * Peripheral nerves - neuropathy
160
late complications of DM variabilty
Great variability among patients in: * Time of onset * Severity * Organs involved
161
what can delay onset of DM complications
Tight glycemic control delays onset
162
late DM complcations most likely to be seen in what tisses?
* Arteries (macrovascular changes) * Basement membrane of small vessels (microangiopathy) * Kidneys (diabetic nephropathy) * Retina (diabetic retinopathy) * Nerves (diabetic neuropathy)
163
most common cause of death in DM
MI
164
# seen with what dx? result of this? hyaline artiolosclerosis seen where?
seen with DM * * Kidneys * Leads to Hypertension
165
microangiopathy of DM
* Thickened Basement membranes (but still leaky) * Nephropathy, Retinopathy, Neuropathy,
166
Acanthosis Nigricans
* 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
seen with? can indicate?
Acanthosis Nigricans, seen with obesity and diabetes can indicate internal malignancy
168
# infections? healing? gingiva? xero? parotid? oral complications of DM
169
mucomycosis (zygomycosis)
170
# change in fucntion? key to this? liver regen capacity?
* 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
functions of liver
metabolic syn plasma pro storage degrade/detox exocrine endocrine
172
metabolic liver function
glucose homeostasis
173
plasma pro made by liver
Albumin, VLDL, LDL, PT, Fibrinogen
174
what can be stored in liver
* Glycogen * Triglycerides * Iron, Copper * Vitamins- A, D, K
175
# phases? detox function of liver
176
exocrine function of liver
bile
177
endocrine fucntions of liver
* D3 to 25-hydroxy-cholecalciferol * T4 to T3 (active) * GHRH * Insulin & glucagon degradation
178
# what chemical? infection? dx? Fe? IS? idiopathic? Causes of Cirrhosis
* ETOH (alc) * Infection (HBV, HCV) * Biliary disease * Iron overload (Hemochromatosis) * Autoimmune hepatitis * 10% idiopathic
179
# how tissue is effected Cirrhosis Characteristics
* Diffuse fibrosis and conversion of normal architecture into abnormal nodules * Bridging fibrosis * Parenchymal nodules: Micro (3mm);Macro, regeneration * Entire liver architecture effaced
180
Complications of Cirrhosis
* LOF * Portal hypertension * Hepatocellular Carcinoma
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# cells lost? blood dynamics? LOF with cirrhiosis
* Hepatocyte death= Loss of Microvilli * Changes in blood flow with decreased Proteins
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# mechanism/leads to? portal hypertension
* 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
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# physical appearence? venous adaption? spleen? NS? Portal Hypertension Clinical Consequences
* Ascites * Formation of portosystemic venous shunts (liver bypassed) * Congestive splenomegaly * Hepatic encephalopathy (build up of toxins in blood alters NS function)
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# type of fluid? Complications of Cirrhosis: Ascities
* Fluid in the peritoneum (500mL) * Serous fluid
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# what can enhance this? pathogenesis of ascites
* 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
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# skin? albumin? NH? glucose? estrogen? coagulation? s/s of liver failuire
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# dx? possible causes? what are the possible indications of each cause? juandice
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
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Icterus
yellowing of eyes w juandice
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where can juandice be seen orally
ginigiva
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Causes of Liver Disease
* Alcohol related * Drug related * Infectious (HCV) * Metabolic * Neoplasms * Autoimmune
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# types of dx? %chronic liver dx from OH? % deaths due to OH? Alcoholic Liver Disease
* 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
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forms of Drug-induced Liver Disease
* Predictable(intrinsic) * Unpredictable(idiosyncratic) * Toxicity + immune reaction
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tetracycline affect at liver
microvascular fatty liver
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antineoplastic drugs effect at liver
macrovascular fatty change with chriosis and fibrosis
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amanita phalloides (mushroom toxin) effect at liver
diffuse/massive necrosis
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CCl4 at liver
centrilobular necrosis
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ETOH affect at liver
macrovascular change fibrosis and chriosis
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can we distinguish drug induced liver dx
* Drug induced chronic hepatitis is indistinguishable from other causes: 1. Alcoholic liver disease 1. Viral Hepatitis * Need serology to r/o viral
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types of hep
A,B,C,D,E
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transmissions of the dif hep
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HepA * limiting? * carrier state? * immunity? * Vaccine? * Epidemics? * fatalities?
* Self limiting * No carrier state * Life long immunity * Vaccine * Epidemics * Rare fatalities (0.1%)
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# incubation? carrier? increased risk for? vax? HepB
* Prolonged incubation * Chronic carrier state * Increased risk of HCCa * Vaccine- Anti-HBs
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# similar to? risk? related to? HCV
* Similar to HBV, but... * More cirrhosis risk * Used to be transfusion related * IV drug related * Early Tx hopeful for cure
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# needs? chance? HDV
* 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
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# WNL? demographics? deposits where? Hemochromatosis
* 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
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types of hemochromatosis
* Hereditary hemochromatosis * Acquired hemochromatosis
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# inheritence? gene/chr? what is lost? net gain? * Hereditary hemochromatosis
* AR most common * HFE gene on Chr 6p * Regulation of intestinal absorption is lost * Net gain/year of 0.5-1.0 gm
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# associated patholgy? * Acquired hemochromatosis
* Known source of excess iron * Hemolytic anemia associated with ineffective erythropoiesis
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# liver? skin? pancreas? Hemochromatosis can present with?
* Hepatomegaly/dysfunction/Cirrhosis * Pancreatic fibrosis which can lead to DM * Skin pigmentation
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wilson dx genetics
mutation at chr 13
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wilsn dx is a disorder of?
copper metabolism
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where does copper accumulate with wilsons dx
liver, brain, eye
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what is the effect of wilson dx
normal copper uptake, but failure to enter circulation as ceruloplasmin inability to be excreted int bile spills into circulation unbund causing hemolysis
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# age of onset? copper levels? liver? nn? diagnosis of wilson
* Onset prior to age 6 * Elevated hepatic copper, low serum ceruloplasmin, high urinary copper * Acute/Chronic hepatitis * Neuropsychiatric
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neuro changes of wilson
* Behavioral changes * Parkinson-like * Pychosis * Kayser-Fleischer rings
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# demo? associated with? begins as? signs? mito? drugs associated? reye syndrome
* 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?
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neoplasias of liver can be
benign or malignant
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benign neoplasias of the liver
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# most common malignancy? preceeding factor? malignant neoplasias of the liver
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# geographics/demographics? associated pathologies? Hepatocellular Carcinoma (Hepatoma)
* 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)
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gallbladder functions
* Stores bile * 50mL * Releases bile * Fat digestion
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gallbladder lacks ?
muscularis mucosae
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dx of gallbladder
* Cholelithiasis * Cholecystitis * Tumors
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Cholelithiasis possible stones
* Cholesterol stones: Crystalline cholesterol monohydrate * Pigment stones: Bilirubin Calcium salts
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Pathogenesis of Cholesterol Stones at gallbladder
* Supersaturated bile with cholesterol * Gallbladder hypomotility * Accelerated cholesterol nucleation * Crystals trapped by gallbladder mucous hypersecretions
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Pathogenesis of Pigment Stones
* Mixture of abnormal insoluble calcium salts of unconjugated bilirubin and inorganic calcium salts
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Cholecystitis forms
acute and chronic
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# due to? are gallstones oresent? acute cholecystits
* Acute inflammation * Obstruction of the neck or cystic duct * Absence of gallstones
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# due to? absecnce of? what forms? chronic cholecystits
Sequel to repeated bouts of acute cholecystitis * Absence of acute cholecystitis * Gallstones
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possible tumors of gallbladder?
* Carcinoma of the gallbladder * Carcinoma of the extrahepatic bile ducts

Pathology (20 decks)

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