Exam 4 Flashcards
(286 cards)
1
Q
Orthotopic Transplantation
A
- graft is transplanted into its usual anatomic location
2
Q
Heterotopic transplantation
A
- graft is transplanted into a site other than its usual anatomic location
- ex. kidneys placed into lower abdomen
3
Q
Autologous transplantation (autograph)
A
- graft is transplanted back into same individual
- ex.) bone marrow “stem cell rescue”
4
Q
Allogenic transplantation (allograph)
A
- graft is transplanted into a genetically different individual of the same species
5
Q
Syngeneic transplantation
A
- graft is transplanted into a genetically identical individual (transplant between mz twins)
6
Q
Xenogeneic transplantation (xenograft)
A
- graph is transplanted between individuals of different species
- ex. tumor cells into mice, bovine valve
7
Q
Some reasons for organ dysfunction
A
- genetic malformation
- autoimmune cellular destruction
- damage from infection, vascular disease, medications, or toxins
8
Q
What types of immune cells generally responsible for organ rejection?
A
- lymphocytes: coordinate amongst one another to destroy cells deemed abnormal in our bodies
9
Q
Hyperacute rejection
A
- blood supply connected –> graft becomes pink
- seconds later, graft turns pale and fails
- rejection due to pre-existing antibodies (HLAs) in recipient’s bloodstream from B-cells that recognize the proteins in the graft as foreign and bind them
- bound antibodies activate complement & the coagulation cascade
- results in rapid thrombosis in the small vessels of the graft, graft ischemic and fails
10
Q
Human Leukocyte Antigen
A
- aka major histocompatability complex (MHC)
- set of proteins expressed on the surface of cells
- each individual has a unique HLA expression pattern
- haploidentical to each parent
- class-1: expressed on all cell types
- class-2: only certain cell types
- chromosome 6: A,B,C, DR, DQ, DP
11
Q
HLA sensitized by: (3)
A
- previous transplant
- previous blood transfusion
- pregnancy
12
Q
Acute Rejection
A
- stems from T-Cells
- have specific receptors for MHCs; T-cells recognize own and any other different patterned cells are identified as non-self and targeted for destruction
- begins first few weeks after transplant
- highest for acute rejection is 3 months post-transplant
13
Q
Chronic Rejection
A
- T-cell mediated
- T-cell response leads to chronic inflammation in the graft
- chronic inflammatory state activates tissue repair mechs which results in scarring and fibrosis of the graft
- main cause of graft failure
- develops slowly over months and years
- slow progressive decline in graft function
14
Q
Two ways rejection can be mitigated
A
- immunosuppression
- minimizing immunogenicity of the graft by minimizing the difference in blood type antigens (ABO matching) and HLA matching between graft and host
15
Q
3 broad types of drugs given for transplant
A
- cyclosporine
- corticosteroids
- antiproliferative agents
16
Q
Calcineurin blockers
A
- cyclosporin
- peptide secreted by a fungus
- used to mitigate transplant rejection
- inhibit T-cell function
- must be given for lifetime of graft
- delicate balance between too little and too much
17
Q
Corticosteroids
A
- used to mitigate transplant rejection
- broad anti-inflammatory effects
- suppresses activation of B and T cells
18
Q
Antiproliferative agents
A
- Azathioprine, mycophenolate, mofetil
- used to mitigate transplant rejection
- inhibit DNA replication in dividing cells preventing the proliferation of activated T-cells that mediate rejection
- but they prevent proliferation of all dividing cells, not specific
- effects profound on bone marrow
- results in neutropenia, anemia, and thrombocytopenia
19
Q
What transplants does it not matter as much to match HLA and ABO? (2)
A
- corneal transplants
- heart valves
20
Q
Complications of transplant (5)
A
- Rejection
- Graft Dysfunction
- Immunosuppression and Infection
- Immunosuppression and Cancer
- Graft v. Host Disease
21
Q
Graft Dysfunction
A
- often grafts fail as a result of a combination of factors
- fibrosis and scarring from combo of rejection & non-immune mediated injury such as hypertension or infection
- viral, fungal, or bacterial infection in a graft is also a frequent contributor to graft dysfunction
22
Q
primary cause of graft dysfunction in heart transplant
A
- accelerated form of atherosclerosis that occludes coronary vessels
23
Q
primary cause of graft dysfunction in kidney transplant
A
- chronic allograft nephropathy (progressive scarring and hypertension)
24
Q
Immunosuppression and Infection in transplant patients
A
- coricosteroid and bone marrow suppression of antiproliferative drugs increase risk for hospital acquired and community acquired bacterial infections
- transplant patients also prone to viral and fungal infections b/c of T-cell suppression so they can’t be cleared as easily
25
3 viral infections that affect transplant recipients
- Epstein-Barr virus (EBV): causes mono, can resurface with immunosuppression
- cytomegalovirus (CMV)
- BK virus
26
Epstein-Barr virus in transplant individs can lead to
- malignant lymphoma
27
cytomegalovirus in transplant individs can lead to
- graft dysfunction and profound immunosuppression
28
BK virus in transplant individs can lead to
- kidney graft failure (80%)
29
Fungal infections seen in immunosuppressed transplant patients
- pneumonia secondary to pneumocystis jiroveci
- meningitis from cryptococcus neoformans (found in soil)
- soft tissue abscesses from Nocardia
- tissue destruction due to Aspergillus (resp. infection from mold)
30
Immunosuppression and cancer in transplant patients: squamous cell carcinoma
- immunosuppression increases risk for cancer
- squamous cell carcinoma ~50% of all transplant patient cancer
- risk 250x higher than general pop
- very important to limit sun exposure
31
Immunosuppression and cancer in transplant patients: two main types of cancer
- squamous cell carcinoma
| - lymphoma
32
Immunosuppression and cancer in transplant patients: Lymphoma
- malignant prolif of B or T lymphocytes
- called post-transplant lymphoproliferative disorder (PTLD)
- 20% of all small bowel transplants
- combined effect of immunosuppression and EBV
- treatment is REDUCING immunosuppression and administering chemotherapy
33
Graft vs Host Disease
- bone marrow transplants replace our native B and T cells with B and T cells from the graft
- new immune system recognizes the HOST as foreign and attacks the host cells in Graft vs host disease (GVHD)
- most severe effects in skin, mucosal lining of GI tract, and liver
- treatment is immunosuppression
- most patients die from opportunistic infections
34
pre-transplant considerations
- underlying infections
- significant uncontrolled life-limiting medical conditions
- active untreated or untreatable malignancy
- social and psychiatric issues like substance abuse, emotionally instability, history of non-compliance
35
anterior chamber angle
- the angle formed between the cornea and the iris where the aqueous fluid drains from the eye
36
Vitreous
- jelly in back of eye
37
retina
- many specific neural layers creating an electrical signal from light
38
Normal aging changes of the eye
- corneal endothelium is lost (pump cells) which pump fluid out of the cornea; cornea at higher risk of swelling
- we do not regenerate pump cells
- lens also becomes more dense, brunescent, and thicker
39
Fuch's Dystrophy
- loss of pump cells with guttata (lesions)
40
presbyopia
- inability to see as one ages
41
Cataracts general info
- reduced transparency of the crystalline lens NOT a film on the cornea of the eye
- can result in a change in color, change in refractive index, or increase in light scattering
- can cause blindness but it is reversible
- require cutting surgery
42
opacification
- increase in light scattering
43
Cataracts epidemiology
- leading cause of blindness worldwide
- 50 million people affected and 90% in developing countries
- single greatest surgical expense borne by medicare
44
Caracts: Risk Factors
- Increased Age- MOST COMMON (>50% of adults over 65 have cataracts)
- smoking
- diabetes
- trauma to or inflammation of the eye
- exposure to sun and UV rays
- corticosteroid medications
45
Symptoms of Cataracts
- normally slow and painless development
- decreased vision, glare
- myopic shift - 2nd sight
- poor night vision
- halos around objects
- lack of color contrast
- double vision w/ one eye open
46
treatment of cataracts
- surgery is definitive treatment
| - glasses can be used to correct cataract-induced changes in refractive error
47
Age Related Macular Degeneration (AMD)
- gradual deterioration of the central retina (macula) with subsequent loss of function
- major cause of blindness but is usually irreversible
- no preventative measures
- affects only central vision (many patients still ambulate well with a cane)
- dry and wet variety
48
Age related macular degeneration epidemiology
- 20/200 vision or worse in their better eye
- most cases are the dry type
- 3% of people with AMD there is a leaky blood vessel that can be coagulated with a laser (success rate not high)
49
Dry age related macular degeneration
- slow changes over time
- few symptoms at first
- mainly just mild progressive decrease in vision
- endstage has areas with no vision (geographic atrophy)
- treated with vitamins, smoking cessation, and healthy diet
50
cellular level of age related macular degeneration
- choroid separates retina and sclera
- many blood vessels there
- bruch's membrane cells die, retinal pigment epithelium start dying too
51
drusen
- waste products that weaken choroid wall
52
What two supplements reduce likelihood of progression of intermediate and advanced degrees of macular degeneration by 25%
- anti-oxidants and zinc
53
Wet age related macular degeneration
- results from blood or serum leaking from NEWLY FORMED blood vessels beneath the retina which scar and lead to vision problems
- less prevalent than dry, dry can progress to wet but usually progresses to end stage dry
- main presenting symptom is metamorphopsia
- laser or intravitreal injection
- poor prognosis
- limited recovery and high recurrence rate
54
Risk factors for age related macular degeneration
- age (>50)
- cigarette smoking
- family history
- increased exposure to UV rays
- caucasian race and or light colored eyes
- hypertension, cardiovascular disease
- low dietary intake of antioxidants and zinc
55
metamorphopsia
- straight lines look wavy
56
purpose of intravitreal injection
- makes blood vessels shrivel up so they do not leak
57
Glaucoma
- caused by increased pressure in the anterior chamber of the eye because of change in natural flow of aqueous humor out of anterior chamber
- sink analogy
- optic nerve disease
58
Two main types of glaucoma
- open angle
| - closed angle
59
open-angle glaucoma
- increased intraocular pressure b/c of blocked flow
- damages the optic nerve and leads to vision loss
- no signs/symptoms in early stage
- tunnel vision to blindness
- irreversible diminished visual acuity at end stages
- optic nerve is cupped out b/c of increased pressure
- hair in sink, plugged but everything looks fine
60
closed-angle glaucoma
- unrelated to progression of open-angle
- results from the angle of iris obstructing the drainage of the aqueous fluid which increases intraocular pressure
- can result from dilating drops, systemic medications, certain lighting conditions
- muscle ischemia that constricts iris
- opthalmic emergency!
61
symptoms of closed-angle glaucoma
- sudden onset severe eye pain
- unilateral headache
- halos around lights
- nausea and vomiting
- blurred vision
- photophobia (extreme sensitivity to light)
62
treatments for OPEN-angle glaucoma
- drops to lower pressure
- laser to clean "drain"
- surgery to make accessory drain if the drain can't be cleared out
63
risk factors for glaucoma
- increased intraocular pressure (both)
- greater than 60 yrs old (both)
- family history of glaucoma (open angle)
- AA ancestry (open angle)
- far sightedness (closed angle)
64
Diabetic Retinopathy (DR)
- leading cause of blindness under 65
- second leading cause of new blindness
- affects 70% of diabetics 10+ yrs after onset
- response to poor blood glc control that is seen eventually in most individs with diabetes mellitus
- background/non-proliferative and proliferative types
- progressive disease
65
Risk Factors for Diabetic Retinopathy (DR)
- duration of disease
- hyperglycemia (poor control)
- proteinuria (renal disease)
- hypertension
- gender
- race
- genetics
- age at examination
- age at diagnosis
- serum lipids
- pregnancy
- smoking cigarettes
- alcohol use - SES
66
Symptoms of Diabetic Reinopathy
- gradual vision loss
- generalized blurring
- areas of focal vision loss (blotches of black in vision)
67
Non proliferative diabetic retinopathy (NPDR)
- blood vessels in eye become damaged
- hemorrhages
- cotton wool spots (ischemic spots)
- microaneurysms --> leak and impair vision
68
Proliferative diabetic retinopathy (PDR)
- damaged blood vessels (from diabetes) lead to retinal ischemia, which decrease the blood and nutrient supply to the retina
- new blood vessels form which are very fragile and leak, so vision is obscured
- get hemorrhages in the vitreous jelly cavity
- black blotches in vision are clotted blood
69
Major causes of vision loss in DR
- macular edema (NPDR)
| - vitreous hemorrhage (PDR)
70
Treatment and prevention of DR
- laser surgery effective
- regular eye exam
- tight glycemic control
- smoking cessation, BP control, hyperlipidemia control
71
why does laser surgery work for diabetic retinopathy
- kill off majority of outer retina, less retina to need oxygen, less drive to make new blood vessels
72
Ocular Tumors (3 types)
- ocular melanoma
- retinoblastoma
- metastatic/other
73
ocular melanoma
- most common primary ocular tumor in adults
| - can metastasize with fatal results
74
retinoblastoma
- most common childhood ocular tumor
- potentially fatal but if detected early has good prognosis (enucleation and chemotherapy)
- presents with white pupillary reflex
- tumor has rosettes (rose-like cell patterns)
- often necrotic areas b/c tumor not good at getting blood flow
75
white pupillary reflex also called
- leukocoria
| - abnormal white reflection
76
enucleation
- removal of eye that leaves eye muscles intact
77
metastatic/other ocular tumors
- choroidal circulation often leads to metastasis of other cancers
- primary neoplasms can also occur in other ocular structures such as the orbit, lacrimal glands, and eyelids
78
Infectious causes of worldwide blindness
- trachoma
- onchocerciasis/river blindness
- HIV
79
Trachoma
- mycoplasmal conjunctivitis carried by flies
- causes scarring and inward turning of eyelids with eventual corneal scarring
- if caught early can be treated with antibiotics
80
Onchocerciasis/river blindness
- prevalent in sub-saharan africa
| - worm infestation also carried by flies
81
HIV re: blindness
- can itself cause retinopathy, but often opportunistic ocular infections happen
- CMV retinopathy (cytomegaloviral)
- herpes zoster
- herpes simplex
- toxoplasmosis
82
Cytomegalovirus (CMV) retinopathy
- most common serious ocular complication of AIDS
- can lead to total blindness
- controlled with antivirals
- can cause retinal detachment
83
Xerophthalmia
- loss of mucus secreting conjunctival goblet cells caused by childhood vitamin A deficiency
84
Pituitary Gland and parts
- aka hypophysis
- anterior lobe (80% of gland): adenohypophysis
- posterior lobe: neurohypophysis
85
hypophyseal stalk
- connects posterior lobe and the hypothalamus
86
Anterior Lobe
- adenohypophysis
- derives from ectoderm that grew up from the oral cavity of the fetus
- secretes ACTH, Prolactin, growth hormone, TSH, and FSH and LH
- if one cell type missing, cannot make it up with other cell types
87
Corticotropes
- cells of anterior lobe that secrete ACTH which stims the adrenal glands
88
Lactotropes
- cells of anterior lobe that secrete prolactin
89
Somatotropes
- cells of anterior lobe that secrete growth hormone
| - affects bone and liver
90
Thyrotropes
- cells of anterior lobe that secrete TSH
91
Gonadotropes
- cells of anterior lobe that secrete FSH and LH
92
Posterior Lobe
- neurohypophysis
- no hormones made in the posterior lobe! only stored there
- oxytocin and vasopressin are made in the hypothalamus and secreted from the pituitary
93
Hypopituitarism
- deficiency of one or more pituitary hormones
94
Panhypopituitarism
- deficiency of ALL pituitary hormones
95
Benign Craniopharyngioma
- one of the most common pituitary tumors in childhood
- congential cyst-like tumor what causes symptoms by pressure and by destroying some or all of the hormone producing cells in the pituitary
96
Diabetes Insipidus
- vasopressin deficiency
- patients cannot concentrate their urine; drink water and urinate excessively
- caused by gene defect, trauma, or tumor
97
Prolactinoma
- benign pituitary tumor of lactotrophs
- secretes excess prolactin
- symptoms are galactorrhea, headache, impotence, infertility
98
galactorrhea
- milk production
99
Nontoxic goiter
- an enlarged thyroid gland that is not hypofunctioning or hyperfunctioning
- seen in adolescence, pregnancy, and some cases of viral or autoimmune thyroiditis
- often associated with growth spurt
100
Hypothyroidism
- underproduction of thyroid hormones
- may occur with or without a goiter
- causes: congential lesions, hashimoto thyroiditis, surgery, viruses, or drugs like lithium
101
Symptoms of hypothyroidism
- bradycardia
- constipation
- cold intolerance
- dry skin,
- hair loss,
- edema of the extremities,
- abnormal menstruation
102
Hashimoto thyroiditis
- autoimmune thyroid disease
- common in those with down syndrome
- pathogenesis is lymphocytic destruction and circulating antibodies to thyroid peroxidase and thyroglobulin
- metaplasia of follicular epithelial cells
103
Hyperthyroidism
- overproduction of thyroid hormone
- most common form is Graves Disease
- usually associated with goiter or nodule
- usually very anxious
104
symptoms of hyperthyroidism
- tachycardia
- heat intolerance
- restlessness
- irritability
- fatigue (never get into deep sleep)
- diaphoresis (excess sweating)
- diarrhea or frequent stools
- tremor
- weight loss
105
goitrous
- autoimmune
- viral thyroiditis
- lithium
106
Parathyroid gland issues
- all symptoms caused by calcium
- found on back of thyroid gland
- 4-12 glands that secrete parathromone (PTH) to control calcium metabolism
107
Hypoparathryoidism
- caused by DECREASED PTH secretion that leads to LOW calcium levels
- symptoms: seizures, tingling, cramps, stridor
- causes: surgery, autoimmune diesase, congenital syndromes of absence of the parathyroid glands
- muscles cannot contract normallly, neurons cannot transmit as well
108
hyperparathyroidism
- caused by EXCESS PTH production causing HIGH calcium levels
- symptoms: "stones, groans, and abdominal moans" kidney and pancreatic duct stones, psychiatric illness, and abdominal pain
- causes benign tumors, cancer, or hyperplasia of the parathyroid glands
109
primary hyperparathyroidism
- rare in children
| - usually benign
110
Congenital Adrenal Hyperplasia
- genetic, congenital disease in which a person is missing an enzyme in the adrenal cortex pathway
- most common 21 hydroxylase defect (cannot make cortisol or aldosterone) results in ambiguous genitalia and salt wasting in girls or salt wasting in boys
- cortisol deficiency causes body to make very high levels of ACTH causing adrenal glands to enlarge and overproduce androgens
111
adrenal insufficiency means _____
- lack of cortisol
| - life threatening and must be promptly treated w/ glucocorticoids (prednisone) to prevent shock and death
112
Causes of adrenal insufficiency
- enzyme defect
- autoimmunity
- infection
- trauma or surgery
- genetic syndrome
- TREAT FIRST
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Low cortisol leads to
- hypotension
- hypoglycemia
- shock
- vomiting
- weight loss
114
Low aldosterone leads to
- low Na
| - high K
115
Addison Disease
- non-specific, many causes
- adrenal cortex insufficiency
- LIFE THREATENING, treat with glucocorticoids immediately!
- causes are autoimmunity, CAH, adrenal hemorrhages, infection, infarction, oral steroids long term
116
Cushing Syndrome
- excess adrenal cortex hormones
- can be caused by adrenal tumors or taking large doses of corticosteroids
- Cushings DISEASE if excess adrenal hormones are b/c of the pituitary over-producing ACTH
- symptoms: obese trunk with thin extremities, moon facies, purple striae on abdomen, thinning of skin, hypertension, buffalo hump, osteoperosis, facial redness, easy bruising, wounds that don't heal well, menstruation abnormal or absent
- child gain weight but not growing
- high ACTH pigments skin around genitals, lips, scars, and creases
117
enlarged sella turcica if what?
- if cushings b/c of too much ACTH
118
Autoimmune Polyglandular Syndromes (APS)
-result of destruction of endocrine glands by antibodies and lymphocytic damage as results of HYPO or HYPER function of endoglands
119
APS-1
- triad of mucocutaneous candidiasis, hypoparathyroidism and addison's disease
- weightloss and vomiting follow
- autosomal recessive defect in chromosome 21 in the AIRE gene
120
APS-1
addisons disease plus diabetes mellitus type 1, thyroid disease, and/or pernicious anemia (b-12)
- thyroid disease can be hashimoto or graves
- HLA antigens DR3 and DR4
121
APS can include other diseases such as (5)
- hepatitis
- autoimmune thyroid disease
- intestinal malabsorption
- vitiligo (symmetrical)
- ovarian or testicular failure
122
Type 1 Diabetes Overview
- aka insulin-dependent, juvenile onset
- can occur at any age, peak before age 20
- symptoms caused by ABSOLUTE insulin deficiency
- usually have lost >80% of beta cells at diagnosis
- specific destruction of islet by autoimmune cells (80% of patients have antibodies to insulin)
- T-cell and macrophage response lead to type 1
123
the 3 Ps of Type 1 Diabetes Mellitus
- polyuria (urinating excessively)
- polydipsia (drinking excessive fluids)
- polyphagia (eating increasing amounts)
- caused by fatty acid oxidation and ketone production
124
Genetics of Type 1 Diabetes
- 95% of people have HLA alleles DR3, DR4, or both
- only 60% of population have these alleles
- 95% of those with type 1 don't have another family member with type 1
125
Type 1 Diabetes: Environment (viruses)
- Cowsackie B or retroviruses possibly associated
- congenital rubella
- viruses look similar to b-cells?
- innocent bystander phenomenon
126
Type 2 Diabetes Overview
- gradual onset
- disease of insulin RESISTANCE
- beta cells can't keep up with demands, but insulin may be normal or even high
- most patients overweight
- most common over age 40 but childhood too
- fatigue common symptom, sometimes wounds not healing
- 60% of patients have an affected sibling or parent (can have a defective gene)
127
Type 2 diabetes risk factors
- obese patients with AT LEAST 2 risk factors
- Family History
- Ethnicity
- Hypertension
- Hyperlipidemia
- Acanthosis Nigricans
- Polycystic Ovarian Syndrome
128
Acanthosis Nigricans
- darkening and thickening of the skin
| - result of increased activity of kerantinocytes and melanocytes in response to insulin
129
Screening for Type 2 diabetes
- fasting glc, HgbA1c, or oral glc tolerance test
| - must be confirmed with second test
130
path of type 2 diabetes
- amyloid or fibrosis in the islets of langerhans
131
Gestational Diabetes
- can complicate pregnancies; all women are screened between the 2nd and 3rd trimesters
- controlled with diet and insulin
- untreated leads to very large infants with hypoglycemia, jaundice, resp. failure, or Ca problems
132
What does obesity due in regards to type 2 diabetes?
- decreases the number of insulin receptors/cell
| - weight loss increases the # of insulin receptors/cell
133
Steroid-induced diabetes
- tends to be insulin resistant
- occurs in some patients on hight dose glucocorticoids for reasons such as transplant, asthma, lupus, arthritis
- treated with insulin (2-3x higher than patient with type 1)
134
Chemotherapy Diabetes
- drugs like vincristine can cause temporary or permanent diabetes
135
Chronic Disease Diabetes
- cystic fibrosis, hemochromatosis damage the islets
136
Complications from diabetes (5)
- caused by severity and chronicity of hyperglycemia
- early diagnosis critical for type 2
- Atherosclerosis
- Diabetic Nephropathy
- Retinopathy
- Peripheral Neuropathy
- Infection
137
Diabetic Nephropathy
- thickening of glomerular basement membranes and diminished renal perfusion
- #1 reason for kidney transplantation
138
Retinopathy (Diabetic)
- leading cause of adult blindness
- non-proliferative: change in retinal basement membrane thickening, microaneurysms, hemorrhage
- proliferative: blood vessels grow and fibrosis destroys vision
139
Perifpheral Neuropathy
- impotence, decreased stomach motility, urinary retention, painful burning in hands and feet, loss of position sense or fine touch, loss of pain recognition
140
Paresthesias
- painful burning sensations in hands and feet
| - bilateral
141
DCCT
- NIH trial with 1400 patients
| - tight control of glc significantly reduced the risk of developing neuropathy, nephropathy, or retinopathy
142
Acute Hepatitis
-
143
Anicteric Acute Hepatitus
- influenza-like and digestive symptoms but no jaundice
144
Icteric Acute Hepatitis
- preceded by days to weeks of non-specific symptoms
- malaise, nausea, decreased appetite
- urine then darkens and jaundice follows
145
Cholestatic Acute Viral Hepatitis
- refers to a prolonged (2 months-yr) jaundice and pruritus
| - systemic illness.. can cause variety of problems elsewhere in body like kidney
146
Acute Liver Failure/Fulminant Hepatic Failure
- sudden and severe
- hallmark is development of cognitive problems, change in consciousness, eventually overt coma
- prolonged prothrombin time
147
what are not good indicators of acute liver failure? (2)
- transaminase elevation and jaundice
148
Chronic Hepatitis
- inflammation >6 months
- ongoing inflammation directed towards the hepatocytes
- some genetic causes, some acquired
149
Causes of Chronic Hepatitis
- A: autoimmune, Alcohol
- B: HBV hep B
- C: HCV hep C, Copper overload (Wilson's Disease)
- D: HDV hep D, Drugs
- alpha 1 antitrypsin deficiency
- iron overload (hereditary hemochromatosis)
- nonalcoholic steatohepatitis
- cholestatic liver disease
150
Cirrhosis
- extensive fibrosis, loss of normal liver architecture b/c of scar tissue/collagen deposition
- 3 principle complications: liver failure, portal hypertension, and liver cancer (hepatocellular carcinoma)
151
What does portal hypertension cause?
- splenomegaly
- varices of other veins that feed into the portal vein system (most commonly in esophagus)
- fluid retention in the abdominal cavity (ascites)
- hepatic encephalopathy (confusion)
152
Alcoholic Liver Disease (ALD) (3)
- spectrum:
* Fatty Liver
* Alcoholic Hepatitis
* Cirrhosis
- 15-20k deaths/yr
- risk related to amt consumed, y/n chronic viral hepatitis, obesity, female
153
Steatosis
- Fatty Liver (Alcoholic Liver Disease)
- increased synthesis of FA, fat accumulates on the liver
- no inflammation
- asymptomatic
- reversible w/ abstinence
154
Alcoholic Hepatitis
- typically very heavy drinkers
- ~10% of those with steatosis
- abdominal pain, fever, jaundice, signs of portal hypertension
- extensive inflammation
- hepatocyte ballooning
- fibrosis
- Mallory Bodies
- fatal in severe cases
- suddenly very sick, no clinical syndrome analogous of non-alcoholic variety
155
Cirrhosis
- end stage alcoholic liver disease
- may present even w/o going through severe alcoholic hepatitis
- treatment: NO ALCOHOL, nutrition, transplantation, corticosteroids if severe inflammation
156
Non-Alcoholic Fatty Liver Disease (NAFLD)/ Non-alcoholic steatohepatitus (NASH)
- NAFLD- no inflammation
- NASH - inflammation
- can look indistinguishable from alcoholic variety
- most commonly seen from the "metabolic syndrome"
157
Metabolic Syndrome (NAFLD/NASH)
- three or more of following:
* Waist Circumference large
* BP high
* high glc (type 2 diabetes)
* hyperlipidemia
* high cholesterol
158
steatohepatitis vs steatosis
- steatohepatitis: inflammation
| - steatosis: fatty liver (no inflammation)
159
Mech of NAFLD/NASH
- insulin resistance --> hepatic steatosis --> oxidative stress --> lipid peroxidation --> NASH --> cirrhosis/liver failure/death
160
Treament of NAFLD/NASH
- weight reduction
- avoidance of alcohol
- antioxidants?
- bariatric surgery
- coffee?
- vitamin E?
- Exercise (even independent of weight loss)
161
What is the theory behind coffee and vitamin E treating NASH/NAFLD
- coffee: protective of death from liver disease
| - Vitamin E: anti-inflammatory
162
Viral Hepatitis
- hepatotropic viruses but have affinity for other organs as well!!
- Hepatitis A-E
163
Hep A
- found worldwide
- causes acute hepatitis
- RNA enterovirus
- fecal-oral transmission, 2 wk incubation before jaundice, still in feces before then
- common in areas with poor sanitation
- majority of cases no jaundice (anicteric)
- NEVER BECOMES CHRONIC (no cirrhosis)
- lifetime immunity after infection
- prevention with immune serum globulin; vaccine available
- spontaneous resolution
- causes acute hepatitis
164
Hep C
- "Virus of the Stars"
- leading cause of cirrhosis, hepatocellular carcinoma, and liver transplant
- single stranded, enveloped RNA virus
- prone to mutation
- envelope accounts for diff genos
- principle risk factor is exposure to infected blood (intravenous drug use)
- sexual transmission rare
- currently most common indication for liver transplant but incidence is decreasing
- most proceed to chronic (85%), 25% of chronic develop cirrhosis
- reinfection can occur
- treatment available but expensive ($92k for 12 wks)
165
Hep D
- single stranded RNA virus
- suppresses HBV replication
- Infection in two forms:
* co-infection: HBV and HDV simultaneously. similar course as HBV b/c HDV can only replicate when HBsAg is being synthesized
* superinfection: occurs in patient later in the course of HBV.. worsening of hepatitis, may lead to fulminant (sever and sudden) course
166
Hep E
- most common in Asia, Africa, Middle East
- single stranded, RNA virus
- transmitted via sewage contaminated water
- enterically transmitted (fecal-oral)
- clinical course similar to A and outbreaks related to poor sanitation
- usually benign except in case of 3rd trimester of pregnancy (25%)
- less virulent in US (no symptoms)
167
Hep B
- double stranded, DNA virus
- core contains HBcAg and HBeAg, surface HBsAg
- major world health problem, rates of infection 20% in some Asian and African areas
- vertical transmission to neonate (asymptomatic but chronic in more than 90%)
- in those exposed as adults (low endemic areas), many acute hepatitis syndrome, but only 10% proceed to chronic
- 2/3 of those in US with HBV were not born in US
- sex, drugs (rock n roll) transmission
- can follow 4 courses (only learned 2)
- chronic can lead to cirrhosis and liver cancer
- vaccine available and antiviral
168
Dane Particle
- in Hep B
- combination of HbsAg and core (HBcAg & HBeAg)
- infectious
169
four courses HBV can take
- acute self-limited hepatitis,
- fulminant/acute liver failure,
- chronic hepatitis,
- chronic, carrier state
170
Acute self-limited HBV
- typically more severe than acute viral hep
- incubation 2 months
- children typically anicteric course
- HBeAg appears after HBsAg and correlates with highest rate of viral replication
- circulating immune complexes cause variety of problems
171
Fulminant Hep B
- relates to an enhanced response of the immune system
| - IgM anti-HBc useful marker
172
Cholelithiasis
- Gallstones: collection of chemicals normally found in bile that ppt out
- most asymptomatic
- biliary colic (spastic pain after eating, right upper abdomen
- bile becomes supersaturated with cholesterol (too much cholesterol or not enough bile salts)
- 10% of US pop
- risk factors: female, >40, fat and rapid weight loss, fertile
- can be pigmented stones
173
Gallstones pigmented
- brown: parasitic infection
| - black: hemolytic anemia
174
Acute Cholecystitis
- infection of bile in the gallbladder due to stone obstructing cystic duct
- causes severe pain in right upper quadrant with radiation to lower shoulder blade
- signs of acute infection: fever, WBC high,
- usually anicteric unless common bile duct also obstructed
- requires removal of gallbladder
175
cholecystectomy
- removal of gallbladder
176
Chronic Cholecysititis
- symptoms often vague and w/o signs of infection
| - may have biliary dyskinesia (lose ability to contract well in response to fatty meal)
177
Choledocholithiasis
- common duct stones "stones on the loose"
- stones loose and can become impacted at opening of the duct
- cause pain, jaundice, infection (ascending cholangitis: infection of bile ducts)
- can be removed endoscopically (ERCP) if not passed naturally or surgically
- fevers often very high, septic shock can occur, low bp
- elevated bilirubin
178
Hereditary Hemochromatosis
- relatively common autosomal recessive
- too much iron absorbed from the gut and is stored all over the body
- causes cirrhosis, diabetes, heart failure, skin bronzing, testicular failure, thyroid, joints
- mutation in the HFE gene
- treatment is blood letting (phlebotomy)
179
Wilson's Disease
- rare, autosomal recessive disorder
- copper buildup in liver (causing cirrhosis), eyes and brain
- treated by binding copper with chelating agent and removing by urine
180
Hepatocellular carcinoma
- extremely rare in normal liver
- HBV predominant risk worldwide
* can occur outside cirrhosis
- cirrhosis is risk otherwise
- HCV, alcohol, hemocromatosis, NASH...
- treatment: surgery, transplant, ablation,
181
Lower Esophageal Sphincter
- NOT a muscular ring
- prevents reflux of stomach contents
- lower 2/3 of esophagus is smooth muscle only
182
Gastroesophageal Reflux Disease (GERD)
- acid from stomach, combined with pepsin & bile, reflux into the esophagus causing pain and inflammation
- can cause metaplasia
- heart burn classic symptom; feeling like something stuck in esophagus
- atypical: laryngitis, asthma, pneumonia, loss of dental enamel
183
pyrosis
- heart burn
184
acid brash
- reflux into esophagus
185
Hiatal Hernia
- condition where upper aspect of stomach is pulled up into chest
- weakens lower esophageal sphincter
- stomach over-distension one of reasons this occurs
186
3 long term complications of GERD from chronic inflammation
- Strictures
- Barrett's Esophagus
- Adenocarcinoma
187
Strictures
- scarring of the esophagus inhibits its motor function and eventually causes significant narrowing
- leads to dyspagia (difficult swallowing); need to put in esophageal dilator
188
Barrett's Esophagus
- chronic damage to lining of esophagus leads to mucosa changing from squamous cell to columnar epithelium
- risk of transforming into cancer
- barrett's esophagus itself does not cause symptoms
189
GERD therapy
- acid suppression
- lifestyle changes
- weight loss
- surgery
190
Adenocarcinoma
- mainly what Americans are affected with
- almost all occurs in setting of Barrett's esophagus
- long term survival is low 20% at 5 yrs
- dysphagia symptom
- tumor is large before presenting symptoms
191
Squamous Cell Cancer of the Esophagus
- worldwide most common esophageal cancer
- low US incidence
- dysphagia most common presenting symptom
- 5 yr survival 10%
192
Non cardiac chest pain
- disorganized, spontaneous contraction of the esophagus
- causes pain that mimicks heart attack
- often due to GERD
193
Achalasia
- problems with foods and liquids right away
- LES loses its ability to relax as a bolus of food travels down the esophagus
- peristalsis above the LES is lost and esophagus bags out
- loss of nerve body cells
- everything fermenting in the esophagus (bad breath)
- treatment: nitrates, botox, dilation,
194
odynophagia
- painful swallowing
195
parietal cells produce what?
- HCl
196
chief cells produce
- pepsinogen
197
prostaglandins make what?
- aid in mucus production, prevent ulceration
198
Peptic Ulcer Disease
- break in the mucosa of the stomach or duodenum
- low mortality
- caused by: smoking, NSAIDs, O blood, stress, helicobacter pylori
- 99% duodenum ulcers benign, gastric mostly also benign
- diagnosis: urea breath test, stool antigen, histopathology
- symptoms: pain, bleeding, hematemesis (vomiting of blood)
199
Helicobacter pylori
- bacteria creates cloud of ammonia which neutralizes acid with enzyme urease
200
hematemesis
- vomiting of blood
201
hematemesis melano
- vomiting black blood
202
hematemesis meatochezia
- vomiting red blood
203
Peptic Ulcer disease treatment
- acid suppression
| - get rid of offending agents
204
Gastritis 2 types
erosive (acute) and Non-erosive (chronic)
| - in stomach
205
Erosive Gastritis
- Acute
- erosions, hemorrhages, ulcers
- NSAIDs most common cause
- stress from trauma, critical illness, and incapacitation
- presents as abdominal pain, severe hemorrhage, anemia
- treat with acid suppression medication
206
Non-Erosive Gastritis
- Chronic
- spectrum
- mild chronic inflammation to severe atrophy
- can be autoimmune, associated with b12 anemia and achlorhyria
- can lead to intestinal metaplasia, precursor to gastric cancer
207
Adenocarcinoma
- tumor of the UGI tract
- significant problem in Japan, in last 60 yrs went from most common cancer in men to a less common cancer
- risk factors H. pylori, diets high in meat and smoked foods, increased age, low SES, tobacco
- no symptoms early; eventual weight loss, nausea, and abdominal pain develop
208
Malignant Lymphoma
- tumor of the UGI tract
- mimics gastric adenocarcinoma
- stomach most common extra-nodal non-hodgkin lymphoma
209
MALT
Mucosa Associated Lymphoid Tissue
- lymphoma of the stomach associated with H. pylori
- for early tumors, clearing HP cures tumor
210
exocrine pancreas cells
| endocrine pancreas cells
- exocrine pancreas: acinar cells which produce digestive enzymes and bicarbonate
- endocrine pancreas: islet cells which produce insulin and glucagon
211
Acute Pancreatitis
- acinar cells of exocrine become inflamed
- large spectrum of symptoms: nothing to hemorrhage and necrosis of cells
- trypsin activates the zymogens in the pancreas, pancreas is self-digested
- two major players: alcohol and gallstones
212
Alcohol and acute pancreatitis
- up to 2/3 of acute pancreatitis due to alcohol
| - may stimulate increased secretion from the pancreas while causing the sphincter of oddi to spasm
213
Gallstones and acute pancreatitis
- 1/3 to 1/2 of all cases associated with gallstones
| - as stones pass through common bile duct cause temporary obstruction of pancreatic duct
214
complications of acute pancreatitis
- inflammation causes fluid to collect in and around the gland
- fluid organize into a collection called pseudocyst
- pseudocyst puts pressure on stomach or duodenum and cause obstructive symptoms
- can also become infected
- can also necrose and abscess can form
215
Chronic Pancreatitis
- chronic inflammation leads to fibrosis, loss of functional cells, and deformities of the ducts
- caused by alcohol, cystic fibrosis, hypertriglyceridemia, idopathic
- presents as pain, malabsorption and weight loss, diabetes
216
Adenocarcinoma of the Pancreas
- 4th leading cancer in men and 5th in women
- early symptoms non-specific, usually not found until it's incurable
- smoking, alcohol, chronic pancreatitis, high fat diet risk factors
- found in head of pancreas in 60% of cases
- Painless jaundice classic presentation for advanced pancreatic cancer, commonly vague pain, weight loss
- therapy: curative surgery- whipple; biliary bypass, chemo, radio, celiac plexus nerve block
217
Type 2 muscle fibers
- dark with high pH
- white fibers
- fast glycolytic
- quick actions
218
Type 1 muscle fibers
- dark with low pH
- red fibers
- slow oxidative
- long distances
219
do most muscles have more type 1 or 2 fibers?
- most have more type II than type I
220
connective tissue around vesicles in muscles:
perimecium
221
Neurogenic atrophy
- group of disorders that lead to atrophy of skeletal muscles
- pattern of "group atrophy"
- one group of fibers dies, is replaced by other type
- eventually adipose and fibrous tissue may replace lost muscle fibers (late phenon)
- ex. ALS, diabetes, trauma
222
Myopathies
- problem with muscle itself
223
Musclar Dystrophy: Progressive (Duchenne) muscular dystrophy
- genetic loss or abnormality in the contractile proteins in the muscles resulting in weakness
- sex-linked, recessive disorder affects male children
- loss of contractile protein dystrophin
- serum enzymes elevated
- mortality around age 20
- classify based on pattern of inheritance, severity of weakness, distribution
- muscle necrosis, fiber loss, inflammation, fibrosis
224
dystrophin
- anchors actin to cell membrane
- no dystrophin, cell membrane breaks down
- muscle undergoes atrophy
225
Peripheral nerve disorder etiologies
- traumatic (most common)
- metabolic (acquired; diabetes) & toxic (50%)
- inflammation, hereditary next most common
226
perinerium
- connective tissue that surround nerve vesicles
227
epineurium
- connective tissue that combines all the vesicles of nerve fibers together; has all the major blood vessels
228
endoneurium
- in between individual nerve fibers
229
Axonal Degeneration
- peripheral nervous system injury
- results from mechanical insults
- Wallerian degeneration
- as debris from severed nerve removed, nerve starts sprouting
- if it reaches destination of original nerve, will synapse
- Schwann cells will remyelinate but with increased number of Schwann cells.. conduction velocity down
- closed injuries more likely to regenerate than open injuries ( penetrating wounds)
230
traumatic neuroma
- found in penetrating axonal peripheral nervou system injuries
- often result of trauma
- aberrant regenerative sprouting
- scar tissue buildup
- connective tissue sheath stays intact
- painful whenever compressed
231
axonal cluster
- multiple axonal processes go through tunnel
| - axonal cluster
232
if small myelin around large axon
- know remyelinatin occurred
233
arterial circle
- internal carotids and vertebral arteries
234
internal carotids what circulation
- anterior
235
vertebral arteries what circulation
- posterior
236
cerebral hemisphere supplied by what circulation
- anterior
237
anterior cerebral artery supply what surface of the brain
- frontal and parietal lobe on medial surface
| - slight lateral surface
238
posterior cerebral artery supply what surface of the brain-
- temporal lobe and occipital lobe on medial surface
| - slight lateral surface
239
middle cerebral artery supplies what surface of the brain
- most of the lateral surface
240
border zone
- aka watershed
- region of brain receiving blood from two diff vessels (still right amt of blood)
- lateral surface
241
Small intestine overview
- duodenum (25cm)
- jejunum
- illeum
- surface area of tennis court
- total length 3.5-6.5 meters
- primary site of digestion and nutrient absorption
242
Colon overview
- absorption of water and electrolytes
| - illeocecal valve opens to the cecum
243
Haustra
- folds of circular muscle that create sac-like segments along the colon
244
GALT
- GI associated Lymphoid tissue
| - 25% the weight of the GI tract
245
Diarrhea
- increase in stool volume or frequency or a decrease consistency
- occurs when carbohydrates or minerals create an osmolar gap and water follows into the lumen or toxins in the body
246
Lactose Intolerance
- inability to break down lactose
- causes diarrhea, gas, and abdominal pain
- generally all animals lose the ability to make lactase around time of weaning
- can take lactase enzyme supplements
247
Celiac Disease (Sprue)
- autoimmune disorder to proteins glutenins and gliandins
- leads to severe chronic diarrhea containing large volumes of fat (steatorrhea)
- associated with weight loss, anemia, and death
- food hypersensitivity
- flattening of normal folds in small intestine (mostly upper part)
- increased epithelial lymphocytes
- CD trio: environ trigger, genetic risk (DQ8, DQ2), leaky gut
- diagnosis by screening antibody test, very sensitive
248
Inflammatory Bowel Disease (IBD)
- chronic inflammation of the bowel
- familial occurence
- interplay between genetics, environment, immune dysregulation
- disease of young adults
- 2 specific types: Chron's and Ulcerative Colitis
249
Hygiene hypothesis
- people in areas that are dirtier are less likely to get Inflammatory bowel disease
- gut is working all the time, building up their gut biome
250
Chronic Ulcerative Colitis
- young adults, 30s
- disease of the lining or mucosa of the colon
- bloody diarrhea, frequent, small bowel movements
- crypt abscess
- >15 yrs with disease at high risk for colon cancer
- sever rapid progression: toxic megacolon
251
Toxic Megacolon
- severe, rapid progression of Ulcerative Colitis`
252
Crohn's Disease
- adolescents and young adults
- can affect any part of the GI tract but most common in terminal illeum and right side of colon
- involves full thickness of wall, early lesions found
- fistulae can form from bowel to bladder, bowel to vagina, or bowel to skin
- very painful
- fever, abdominal pain, diarrhea
- granulomas typically found (what distinguishes it from UC)
- therapy: induce & maintain remission by prednisone, surgery, anti-tnf
- risk of colon cancer increased
253
Presentation of Crohn's disease
- colon alone
- illeocolic
- scarring
- colon alone: like UC
- illeocolic: like apendicitis
- scarring: like a bowel obstructio
254
Diverticulosis
- 80% asymptomatic
- formation of mucosal outpouchings of the lining of the large bowel
- 1 in 3 people over 50
- caused by low dietary fiber and high pressure to move stool forward
- complications: diverticulitis, bleeding
255
Diverticulitis
- complication of diverticulosis
- stool and bacteria trapped in pockets leading to low grade infection
- abscess formation
- chronic infections lead to scarring
- left lower quad pain, high wbc count
256
Bleeding with diverticulosis
- small arteries rupture and lead to severe, painless, lower GI bleeding
- blood thinners increase severity
- other common cause is angiodysplasia: small vascular malformation
257
polyp
- mass that protrudes into the lumen of the gut
- adenomatous polyps (adenomas) can progress to cancer
- many others that don't
258
adenoma-carcinoma hypthesis
- polyps accumulate a number of genetic mutations over time that lead to cancer
259
colorectal cancer
- more common in West (low fiber, high fat diets)
- may cause hidden bleeding (ocult), but generally silent
- screening yearly after age 50
- advanced colon cancer may cause gross bleeding, obstruction, perforation, or fistula
- Dukes staging system
260
Dukes staging system
- A: tumors confined to bowel wall (muscular layer)
- B: cancer extends beyond bowel wall
- C: lymph node involvement
- D: metastasis
261
Family Cancer Syndromes GI
- 20% due to direct genetic influence
- Familial Adenomatous Polyposis (FAP; lynch syndrome)
- Hereditary non-polyposis colon cancer
262
Familial Adenomatous Polyposis (FAP) (Lynch Syndrome)
- autsomal dominant
- defect on chromosome 5
- colon cancer inevitable by age 40
- thousands of polyps develop
263
Hereditary Non-polyposis Colon Cancer
- patients with small numbers of polyps but clustering of colon, pancreas, ovar, and uterus cancers
- defect in the mis-match repair gene
264
Cerebrovascular Accident /Stroke
- general sudden onset of focal neurologic deficit
- most are due to embolism or spontaneous, massive hemorrhage
- 40-80 yrs, more common in males
- third leading cause of death, most common neurologic disease
- 42% of victims have reoccurrence
- symptoms: paralysis, sensory loss, speech deficits, headache, vomiting, coma
- more beneficial to talk about patterns: 3 common patterns of injury
265
3 common patterns of injury with cerebrovascular accident
- 73% infarcts (thromboembolisms, hypoxia, ischemia)
- 19% intraparenchymal hemorrhages (secondary to hypertension)
- 7% subarachnoid hemorrhages (rupture of aneurysms)
266
what area of circulation most affected by hypertension?
- border zone
267
Arteriosclerosis vs Atherosclerosis vs Ateriolosclerosis
- ateriosclerosis: generic hardening of arteries
- arteriosclerosis: large & medium arteries; hyperlipidemia; causes large infarcts
- arteriolosclerosis: small arteries and arterioles; CAUSES hypertension; also cause hemorrhages in brain
268
Hypoxia
- decreased amount of oxygen in perfused tissue regardless of pressure
- can lead to ischemia
269
Ischemia
- decrease in blood supply
| - may be local or generalized
270
Infarct
- necrosis of tissue secondary to ischemia/hypoxia
| - some strokes transient and reversible; don't result in infarcts
271
Cerebral emobli
- occlusion of a blood vessel by any material which is transported through the circulation to another site
- commonly from thrombosis that breaks off in leg
- most common cause of infarction
272
Thrombosis
- occlusion of vessel in situ
| - secondary to formation of a blood clot in an already damaged artery by atherosclerosis
273
Hemorrhage
- usually associated with hypertension
274
Blood-Brain Barrier
- brain has tight junctions to prevent movement of large particles from blood into the brain
- protects brain from excess fluids that would follow salt
- problem is restricts passage of therapeutic agents
275
Infarcts
- due to thrombosis, embolism, hypotension, or hypoxia
| - small area of dead tissue
276
transient ischemic attacks
- loss of speech days or weeks prior to stroke
277
Intraparenchymal hemorrhage
- bleeding w/in brain parenchyma
| - hypertensive hemorrhage most common cause
278
subarachnoid hemorrhage
- non-traumatic most commonly due to rupture of saccular aneurysm
279
sacular/berry aneurysm
- disease of adults
- more common in women
- congenital defect
- 90% found in anterior portion of the arterial circle
- subarachnoid hemorrhage is most common
- also intracranial hemorrhage (associated with rapid death)
- expanding intracranial masses (mimic pituitary tumors)
- 30% patients die
280
Brain Herniation
- brain is encased in rigid bony vault
- when increase in mass of brain for any reason (hemorrhage, edema, abscess) brain is pushed into foramen magnum and results in compression of the brain stem
281
Parahippocampal/uncal herniation
- entire part of parahippocampal gyrus herniates through the opening of the tentorium causing compression of the brainstem
- followed by hemorrhage
282
Cerebellar Tonsilar Herniation
- cerebellar tonsils herniate through the foramen magnum compressing the medulla
- can result in death b/c of interference with cardiac and respiratory centers in brainstem
283
Epidural Hemorrhage
- one of the most acute medical emergencies
- head injury fractures temporal bone and ARTERY is torn
- blood accumulates rapidly through epidural space
- most lethal within a few hours
- classically, lucid interval of 30 minutes to several hours following brief unconsciousness
- then patient rapidly deteriorates; dilated pupil on ipsilateral side
284
Subdural Hemorrhage
- 50% of fatal cases of head injuries
- may be nontraumatic
- more common in males, very young and very old
- most common source is rupture in VEINS
- may be acute, subacute, or chronic
285
why subdural hemorrhage in elderly
- bridging veins very tight
286
why subdural hemorrhage in young?
- sign of child abuse
