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Path 404 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Orthotopic Transplantation

A
  • graft is transplanted into its usual anatomic location
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2
Q

Heterotopic transplantation

A
  • graft is transplanted into a site other than its usual anatomic location
  • ex. kidneys placed into lower abdomen
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3
Q

Autologous transplantation (autograph)

A
  • graft is transplanted back into same individual

- ex.) bone marrow “stem cell rescue”

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4
Q

Allogenic transplantation (allograph)

A
  • graft is transplanted into a genetically different individual of the same species
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5
Q

Syngeneic transplantation

A
  • graft is transplanted into a genetically identical individual (transplant between mz twins)
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6
Q

Xenogeneic transplantation (xenograft)

A
  • graph is transplanted between individuals of different species
  • ex. tumor cells into mice, bovine valve
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7
Q

Some reasons for organ dysfunction

A
  • genetic malformation
  • autoimmune cellular destruction
  • damage from infection, vascular disease, medications, or toxins
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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
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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
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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
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11
Q

HLA sensitized by: (3)

A
  • previous transplant
  • previous blood transfusion
  • pregnancy
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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
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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
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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
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15
Q

3 broad types of drugs given for transplant

A
  • cyclosporine
  • corticosteroids
  • antiproliferative agents
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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
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17
Q

Corticosteroids

A
  • used to mitigate transplant rejection
  • broad anti-inflammatory effects
  • suppresses activation of B and T cells
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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
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19
Q

What transplants does it not matter as much to match HLA and ABO? (2)

A
  • corneal transplants

- heart valves

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20
Q

Complications of transplant (5)

A
  • Rejection
  • Graft Dysfunction
  • Immunosuppression and Infection
  • Immunosuppression and Cancer
  • Graft v. Host Disease
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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
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22
Q

primary cause of graft dysfunction in heart transplant

A
  • accelerated form of atherosclerosis that occludes coronary vessels
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23
Q

primary cause of graft dysfunction in kidney transplant

A
  • chronic allograft nephropathy (progressive scarring and hypertension)
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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
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25
Q

3 viral infections that affect transplant recipients

A
  • Epstein-Barr virus (EBV): causes mono, can resurface with immunosuppression
  • cytomegalovirus (CMV)
  • BK virus
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26
Q

Epstein-Barr virus in transplant individs can lead to

A
  • malignant lymphoma
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27
Q

cytomegalovirus in transplant individs can lead to

A
  • graft dysfunction and profound immunosuppression
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28
Q

BK virus in transplant individs can lead to

A
  • kidney graft failure (80%)
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29
Q

Fungal infections seen in immunosuppressed transplant patients

A
  • 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)
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30
Q

Immunosuppression and cancer in transplant patients: squamous cell carcinoma

A
  • 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
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31
Q

Immunosuppression and cancer in transplant patients: two main types of cancer

A
  • squamous cell carcinoma

- lymphoma

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32
Q

Immunosuppression and cancer in transplant patients: Lymphoma

A
  • 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
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33
Q

Graft vs Host Disease

A
  • 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
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34
Q

pre-transplant considerations

A
  • 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
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35
Q

anterior chamber angle

A
  • the angle formed between the cornea and the iris where the aqueous fluid drains from the eye
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36
Q

Vitreous

A
  • jelly in back of eye
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37
Q

retina

A
  • many specific neural layers creating an electrical signal from light
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38
Q

Normal aging changes of the eye

A
  • 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
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39
Q

Fuch’s Dystrophy

A
  • loss of pump cells with guttata (lesions)
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40
Q

presbyopia

A
  • inability to see as one ages
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41
Q

Cataracts general info

A
  • 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
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42
Q

opacification

A
  • increase in light scattering
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43
Q

Cataracts epidemiology

A
  • leading cause of blindness worldwide
  • 50 million people affected and 90% in developing countries
  • single greatest surgical expense borne by medicare
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44
Q

Caracts: Risk Factors

A
  • 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
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45
Q

Symptoms of Cataracts

A
  • 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
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46
Q

treatment of cataracts

A
  • surgery is definitive treatment

- glasses can be used to correct cataract-induced changes in refractive error

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47
Q

Age Related Macular Degeneration (AMD)

A
  • 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
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48
Q

Age related macular degeneration epidemiology

A
  • 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)
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49
Q

Dry age related macular degeneration

A
  • 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
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50
Q

cellular level of age related macular degeneration

A
  • choroid separates retina and sclera
  • many blood vessels there
  • bruch’s membrane cells die, retinal pigment epithelium start dying too
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51
Q

drusen

A
  • waste products that weaken choroid wall
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52
Q

What two supplements reduce likelihood of progression of intermediate and advanced degrees of macular degeneration by 25%

A
  • anti-oxidants and zinc
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53
Q

Wet age related macular degeneration

A
  • 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
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54
Q

Risk factors for age related macular degeneration

A
  • 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
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55
Q

metamorphopsia

A
  • straight lines look wavy
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56
Q

purpose of intravitreal injection

A
  • makes blood vessels shrivel up so they do not leak
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57
Q

Glaucoma

A
  • 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
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58
Q

Two main types of glaucoma

A
  • open angle

- closed angle

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59
Q

open-angle glaucoma

A
  • 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
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60
Q

closed-angle glaucoma

A
  • 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!
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61
Q

symptoms of closed-angle glaucoma

A
  • sudden onset severe eye pain
  • unilateral headache
  • halos around lights
  • nausea and vomiting
  • blurred vision
  • photophobia (extreme sensitivity to light)
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62
Q

treatments for OPEN-angle glaucoma

A
  • drops to lower pressure
  • laser to clean “drain”
  • surgery to make accessory drain if the drain can’t be cleared out
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63
Q

risk factors for glaucoma

A
  • increased intraocular pressure (both)
  • greater than 60 yrs old (both)
  • family history of glaucoma (open angle)
  • AA ancestry (open angle)
  • far sightedness (closed angle)
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64
Q

Diabetic Retinopathy (DR)

A
  • 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
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65
Q

Risk Factors for Diabetic Retinopathy (DR)

A
  • 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
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66
Q

Symptoms of Diabetic Reinopathy

A
  • gradual vision loss
  • generalized blurring
  • areas of focal vision loss (blotches of black in vision)
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67
Q

Non proliferative diabetic retinopathy (NPDR)

A
  • blood vessels in eye become damaged
  • hemorrhages
  • cotton wool spots (ischemic spots)
  • microaneurysms –> leak and impair vision
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68
Q

Proliferative diabetic retinopathy (PDR)

A
  • 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
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69
Q

Major causes of vision loss in DR

A
  • macular edema (NPDR)

- vitreous hemorrhage (PDR)

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70
Q

Treatment and prevention of DR

A
  • laser surgery effective
  • regular eye exam
  • tight glycemic control
  • smoking cessation, BP control, hyperlipidemia control
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71
Q

why does laser surgery work for diabetic retinopathy

A
  • kill off majority of outer retina, less retina to need oxygen, less drive to make new blood vessels
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72
Q

Ocular Tumors (3 types)

A
  • ocular melanoma
  • retinoblastoma
  • metastatic/other
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73
Q

ocular melanoma

A
  • most common primary ocular tumor in adults

- can metastasize with fatal results

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74
Q

retinoblastoma

A
  • 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
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75
Q

white pupillary reflex also called

A
  • leukocoria

- abnormal white reflection

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76
Q

enucleation

A
  • removal of eye that leaves eye muscles intact
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77
Q

metastatic/other ocular tumors

A
  • 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
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78
Q

Infectious causes of worldwide blindness

A
  • trachoma
  • onchocerciasis/river blindness
  • HIV
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79
Q

Trachoma

A
  • mycoplasmal conjunctivitis carried by flies
  • causes scarring and inward turning of eyelids with eventual corneal scarring
  • if caught early can be treated with antibiotics
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80
Q

Onchocerciasis/river blindness

A
  • prevalent in sub-saharan africa

- worm infestation also carried by flies

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81
Q

HIV re: blindness

A
  • can itself cause retinopathy, but often opportunistic ocular infections happen
  • CMV retinopathy (cytomegaloviral)
  • herpes zoster
  • herpes simplex
  • toxoplasmosis
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82
Q

Cytomegalovirus (CMV) retinopathy

A
  • most common serious ocular complication of AIDS
  • can lead to total blindness
  • controlled with antivirals
  • can cause retinal detachment
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83
Q

Xerophthalmia

A
  • loss of mucus secreting conjunctival goblet cells caused by childhood vitamin A deficiency
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84
Q

Pituitary Gland and parts

A
  • aka hypophysis
  • anterior lobe (80% of gland): adenohypophysis
  • posterior lobe: neurohypophysis
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85
Q

hypophyseal stalk

A
  • connects posterior lobe and the hypothalamus
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86
Q

Anterior Lobe

A
  • 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
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87
Q

Corticotropes

A
  • cells of anterior lobe that secrete ACTH which stims the adrenal glands
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88
Q

Lactotropes

A
  • cells of anterior lobe that secrete prolactin
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89
Q

Somatotropes

A
  • cells of anterior lobe that secrete growth hormone

- affects bone and liver

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90
Q

Thyrotropes

A
  • cells of anterior lobe that secrete TSH
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91
Q

Gonadotropes

A
  • cells of anterior lobe that secrete FSH and LH
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92
Q

Posterior Lobe

A
  • neurohypophysis
  • no hormones made in the posterior lobe! only stored there
  • oxytocin and vasopressin are made in the hypothalamus and secreted from the pituitary
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93
Q

Hypopituitarism

A
  • deficiency of one or more pituitary hormones
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94
Q

Panhypopituitarism

A
  • deficiency of ALL pituitary hormones
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95
Q

Benign Craniopharyngioma

A
  • 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
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96
Q

Diabetes Insipidus

A
  • vasopressin deficiency
  • patients cannot concentrate their urine; drink water and urinate excessively
  • caused by gene defect, trauma, or tumor
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97
Q

Prolactinoma

A
  • benign pituitary tumor of lactotrophs
  • secretes excess prolactin
  • symptoms are galactorrhea, headache, impotence, infertility
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98
Q

galactorrhea

A
  • milk production
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99
Q

Nontoxic goiter

A
  • 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
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100
Q

Hypothyroidism

A
  • underproduction of thyroid hormones
  • may occur with or without a goiter
  • causes: congential lesions, hashimoto thyroiditis, surgery, viruses, or drugs like lithium
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101
Q

Symptoms of hypothyroidism

A
  • bradycardia
  • constipation
  • cold intolerance
  • dry skin,
  • hair loss,
  • edema of the extremities,
  • abnormal menstruation
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102
Q

Hashimoto thyroiditis

A
  • 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
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103
Q

Hyperthyroidism

A
  • overproduction of thyroid hormone
  • most common form is Graves Disease
  • usually associated with goiter or nodule
  • usually very anxious
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104
Q

symptoms of hyperthyroidism

A
  • tachycardia
  • heat intolerance
  • restlessness
  • irritability
  • fatigue (never get into deep sleep)
  • diaphoresis (excess sweating)
  • diarrhea or frequent stools
  • tremor
  • weight loss
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105
Q

goitrous

A
  • autoimmune
  • viral thyroiditis
  • lithium
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106
Q

Parathyroid gland issues

A
  • all symptoms caused by calcium
  • found on back of thyroid gland
  • 4-12 glands that secrete parathromone (PTH) to control calcium metabolism
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107
Q

Hypoparathryoidism

A
  • 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
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108
Q

hyperparathyroidism

A
  • 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
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109
Q

primary hyperparathyroidism

A
  • rare in children

- usually benign

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110
Q

Congenital Adrenal Hyperplasia

A
  • 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
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111
Q

adrenal insufficiency means _____

A
  • lack of cortisol

- life threatening and must be promptly treated w/ glucocorticoids (prednisone) to prevent shock and death

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112
Q

Causes of adrenal insufficiency

A
  • enzyme defect
  • autoimmunity
  • infection
  • trauma or surgery
  • genetic syndrome
  • TREAT FIRST
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113
Q

Low cortisol leads to

A
  • hypotension
  • hypoglycemia
  • shock
  • vomiting
  • weight loss
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114
Q

Low aldosterone leads to

A
  • low Na

- high K

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115
Q

Addison Disease

A
  • 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
Q

Cushing Syndrome

A
  • 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
Q

enlarged sella turcica if what?

A
  • if cushings b/c of too much ACTH
118
Q

Autoimmune Polyglandular Syndromes (APS)

A

-result of destruction of endocrine glands by antibodies and lymphocytic damage as results of HYPO or HYPER function of endoglands

119
Q

APS-1

A
  • triad of mucocutaneous candidiasis, hypoparathyroidism and addison’s disease
  • weightloss and vomiting follow
  • autosomal recessive defect in chromosome 21 in the AIRE gene
120
Q

APS-1

A

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
Q

APS can include other diseases such as (5)

A
  • hepatitis
  • autoimmune thyroid disease
  • intestinal malabsorption
  • vitiligo (symmetrical)
  • ovarian or testicular failure
122
Q

Type 1 Diabetes Overview

A
  • 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
Q

the 3 Ps of Type 1 Diabetes Mellitus

A
  • polyuria (urinating excessively)
  • polydipsia (drinking excessive fluids)
  • polyphagia (eating increasing amounts)
  • caused by fatty acid oxidation and ketone production
124
Q

Genetics of Type 1 Diabetes

A
  • 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
Q

Type 1 Diabetes: Environment (viruses)

A
  • Cowsackie B or retroviruses possibly associated
  • congenital rubella
  • viruses look similar to b-cells?
  • innocent bystander phenomenon
126
Q

Type 2 Diabetes Overview

A
  • 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
Q

Type 2 diabetes risk factors

A
  • obese patients with AT LEAST 2 risk factors
  • Family History
  • Ethnicity
  • Hypertension
  • Hyperlipidemia
  • Acanthosis Nigricans
  • Polycystic Ovarian Syndrome
128
Q

Acanthosis Nigricans

A
  • darkening and thickening of the skin

- result of increased activity of kerantinocytes and melanocytes in response to insulin

129
Q

Screening for Type 2 diabetes

A
  • fasting glc, HgbA1c, or oral glc tolerance test

- must be confirmed with second test

130
Q

path of type 2 diabetes

A
  • amyloid or fibrosis in the islets of langerhans
131
Q

Gestational Diabetes

A
  • 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
Q

What does obesity due in regards to type 2 diabetes?

A
  • decreases the number of insulin receptors/cell

- weight loss increases the # of insulin receptors/cell

133
Q

Steroid-induced diabetes

A
  • 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
Q

Chemotherapy Diabetes

A
  • drugs like vincristine can cause temporary or permanent diabetes
135
Q

Chronic Disease Diabetes

A
  • cystic fibrosis, hemochromatosis damage the islets
136
Q

Complications from diabetes (5)

A
  • caused by severity and chronicity of hyperglycemia
  • early diagnosis critical for type 2
  • Atherosclerosis
  • Diabetic Nephropathy
  • Retinopathy
  • Peripheral Neuropathy
  • Infection
137
Q

Diabetic Nephropathy

A
  • thickening of glomerular basement membranes and diminished renal perfusion
  • # 1 reason for kidney transplantation
138
Q

Retinopathy (Diabetic)

A
  • leading cause of adult blindness
  • non-proliferative: change in retinal basement membrane thickening, microaneurysms, hemorrhage
  • proliferative: blood vessels grow and fibrosis destroys vision
139
Q

Perifpheral Neuropathy

A
  • impotence, decreased stomach motility, urinary retention, painful burning in hands and feet, loss of position sense or fine touch, loss of pain recognition
140
Q

Paresthesias

A
  • painful burning sensations in hands and feet

- bilateral

141
Q

DCCT

A
  • NIH trial with 1400 patients

- tight control of glc significantly reduced the risk of developing neuropathy, nephropathy, or retinopathy

142
Q

Acute Hepatitis

A

-

143
Q

Anicteric Acute Hepatitus

A
  • influenza-like and digestive symptoms but no jaundice
144
Q

Icteric Acute Hepatitis

A
  • preceded by days to weeks of non-specific symptoms
  • malaise, nausea, decreased appetite
  • urine then darkens and jaundice follows
145
Q

Cholestatic Acute Viral Hepatitis

A
  • refers to a prolonged (2 months-yr) jaundice and pruritus

- systemic illness.. can cause variety of problems elsewhere in body like kidney

146
Q

Acute Liver Failure/Fulminant Hepatic Failure

A
  • sudden and severe
  • hallmark is development of cognitive problems, change in consciousness, eventually overt coma
  • prolonged prothrombin time
147
Q

what are not good indicators of acute liver failure? (2)

A
  • transaminase elevation and jaundice
148
Q

Chronic Hepatitis

A
  • inflammation >6 months
  • ongoing inflammation directed towards the hepatocytes
  • some genetic causes, some acquired
149
Q

Causes of Chronic Hepatitis

A
  • 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
Q

Cirrhosis

A
  • 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
Q

What does portal hypertension cause?

A
  • 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
Q

Alcoholic Liver Disease (ALD) (3)

A
  • spectrum:
  • Fatty Liver
  • Alcoholic Hepatitis
  • Cirrhosis
  • 15-20k deaths/yr
  • risk related to amt consumed, y/n chronic viral hepatitis, obesity, female
153
Q

Steatosis

A
  • Fatty Liver (Alcoholic Liver Disease)
  • increased synthesis of FA, fat accumulates on the liver
  • no inflammation
  • asymptomatic
  • reversible w/ abstinence
154
Q

Alcoholic Hepatitis

A
  • 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
Q

Cirrhosis

A
  • 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
Q

Non-Alcoholic Fatty Liver Disease (NAFLD)/ Non-alcoholic steatohepatitus (NASH)

A
  • NAFLD- no inflammation
  • NASH - inflammation
  • can look indistinguishable from alcoholic variety
  • most commonly seen from the “metabolic syndrome”
157
Q

Metabolic Syndrome (NAFLD/NASH)

A
  • three or more of following:
  • Waist Circumference large
  • BP high
  • high glc (type 2 diabetes)
  • hyperlipidemia
  • high cholesterol
158
Q

steatohepatitis vs steatosis

A
  • steatohepatitis: inflammation

- steatosis: fatty liver (no inflammation)

159
Q

Mech of NAFLD/NASH

A
  • insulin resistance –> hepatic steatosis –> oxidative stress –> lipid peroxidation –> NASH –> cirrhosis/liver failure/death
160
Q

Treament of NAFLD/NASH

A
  • weight reduction
  • avoidance of alcohol
  • antioxidants?
  • bariatric surgery
  • coffee?
  • vitamin E?
  • Exercise (even independent of weight loss)
161
Q

What is the theory behind coffee and vitamin E treating NASH/NAFLD

A
  • coffee: protective of death from liver disease

- Vitamin E: anti-inflammatory

162
Q

Viral Hepatitis

A
  • hepatotropic viruses but have affinity for other organs as well!!
  • Hepatitis A-E
163
Q

Hep A

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
Q

Hep C

A
  • “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
Q

Hep D

A
  • 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
Q

Hep E

A
  • 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
Q

Hep B

A
  • 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
Q

Dane Particle

A
  • in Hep B
  • combination of HbsAg and core (HBcAg & HBeAg)
  • infectious
169
Q

four courses HBV can take

A
  • acute self-limited hepatitis,
  • fulminant/acute liver failure,
  • chronic hepatitis,
  • chronic, carrier state
170
Q

Acute self-limited HBV

A
  • 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
Q

Fulminant Hep B

A
  • relates to an enhanced response of the immune system

- IgM anti-HBc useful marker

172
Q

Cholelithiasis

A
  • 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
Q

Gallstones pigmented

A
  • brown: parasitic infection

- black: hemolytic anemia

174
Q

Acute Cholecystitis

A
  • 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
Q

cholecystectomy

A
  • removal of gallbladder
176
Q

Chronic Cholecysititis

A
  • symptoms often vague and w/o signs of infection

- may have biliary dyskinesia (lose ability to contract well in response to fatty meal)

177
Q

Choledocholithiasis

A
  • 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
Q

Hereditary Hemochromatosis

A
  • 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
Q

Wilson’s Disease

A
  • 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
Q

Hepatocellular carcinoma

A
  • 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
Q

Lower Esophageal Sphincter

A
  • NOT a muscular ring
  • prevents reflux of stomach contents
  • lower 2/3 of esophagus is smooth muscle only
182
Q

Gastroesophageal Reflux Disease (GERD)

A
  • 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
Q

pyrosis

A
  • heart burn
184
Q

acid brash

A
  • reflux into esophagus
185
Q

Hiatal Hernia

A
  • condition where upper aspect of stomach is pulled up into chest
  • weakens lower esophageal sphincter
  • stomach over-distension one of reasons this occurs
186
Q

3 long term complications of GERD from chronic inflammation

A
  • Strictures
  • Barrett’s Esophagus
  • Adenocarcinoma
187
Q

Strictures

A
  • 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
Q

Barrett’s Esophagus

A
  • 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
Q

GERD therapy

A
  • acid suppression
  • lifestyle changes
  • weight loss
  • surgery
190
Q

Adenocarcinoma

A
  • 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
Q

Squamous Cell Cancer of the Esophagus

A
  • worldwide most common esophageal cancer
  • low US incidence
  • dysphagia most common presenting symptom
  • 5 yr survival 10%
192
Q

Non cardiac chest pain

A
  • disorganized, spontaneous contraction of the esophagus
  • causes pain that mimicks heart attack
  • often due to GERD
193
Q

Achalasia

A
  • 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
Q

odynophagia

A
  • painful swallowing
195
Q

parietal cells produce what?

A
  • HCl
196
Q

chief cells produce

A
  • pepsinogen
197
Q

prostaglandins make what?

A
  • aid in mucus production, prevent ulceration
198
Q

Peptic Ulcer Disease

A
  • 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
Q

Helicobacter pylori

A
  • bacteria creates cloud of ammonia which neutralizes acid with enzyme urease
200
Q

hematemesis

A
  • vomiting of blood
201
Q

hematemesis melano

A
  • vomiting black blood
202
Q

hematemesis meatochezia

A
  • vomiting red blood
203
Q

Peptic Ulcer disease treatment

A
  • acid suppression

- get rid of offending agents

204
Q

Gastritis 2 types

A

erosive (acute) and Non-erosive (chronic)

- in stomach

205
Q

Erosive Gastritis

A
  • 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
Q

Non-Erosive Gastritis

A
  • 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
Q

Adenocarcinoma

A
  • 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
Q

Malignant Lymphoma

A
  • tumor of the UGI tract
  • mimics gastric adenocarcinoma
  • stomach most common extra-nodal non-hodgkin lymphoma
209
Q

MALT

A

Mucosa Associated Lymphoid Tissue

  • lymphoma of the stomach associated with H. pylori
  • for early tumors, clearing HP cures tumor
210
Q

exocrine pancreas cells

endocrine pancreas cells

A
  • exocrine pancreas: acinar cells which produce digestive enzymes and bicarbonate
  • endocrine pancreas: islet cells which produce insulin and glucagon
211
Q

Acute Pancreatitis

A
  • 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
Q

Alcohol and acute pancreatitis

A
  • 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
Q

Gallstones and acute pancreatitis

A
  • 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
Q

complications of acute pancreatitis

A
  • 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
Q

Chronic Pancreatitis

A
  • 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
Q

Adenocarcinoma of the Pancreas

A
  • 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
Q

Type 2 muscle fibers

A
  • dark with high pH
  • white fibers
  • fast glycolytic
  • quick actions
218
Q

Type 1 muscle fibers

A
  • dark with low pH
  • red fibers
  • slow oxidative
  • long distances
219
Q

do most muscles have more type 1 or 2 fibers?

A
  • most have more type II than type I
220
Q

connective tissue around vesicles in muscles:

A

perimecium

221
Q

Neurogenic atrophy

A
  • 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
Q

Myopathies

A
  • problem with muscle itself
223
Q

Musclar Dystrophy: Progressive (Duchenne) muscular dystrophy

A
  • 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
Q

dystrophin

A
  • anchors actin to cell membrane
  • no dystrophin, cell membrane breaks down
  • muscle undergoes atrophy
225
Q

Peripheral nerve disorder etiologies

A
  • traumatic (most common)
  • metabolic (acquired; diabetes) & toxic (50%)
  • inflammation, hereditary next most common
226
Q

perinerium

A
  • connective tissue that surround nerve vesicles
227
Q

epineurium

A
  • connective tissue that combines all the vesicles of nerve fibers together; has all the major blood vessels
228
Q

endoneurium

A
  • in between individual nerve fibers
229
Q

Axonal Degeneration

A
  • 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
Q

traumatic neuroma

A
  • 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
Q

axonal cluster

A
  • multiple axonal processes go through tunnel

- axonal cluster

232
Q

if small myelin around large axon

A
  • know remyelinatin occurred
233
Q

arterial circle

A
  • internal carotids and vertebral arteries
234
Q

internal carotids what circulation

A
  • anterior
235
Q

vertebral arteries what circulation

A
  • posterior
236
Q

cerebral hemisphere supplied by what circulation

A
  • anterior
237
Q

anterior cerebral artery supply what surface of the brain

A
  • frontal and parietal lobe on medial surface

- slight lateral surface

238
Q

posterior cerebral artery supply what surface of the brain-

A
  • temporal lobe and occipital lobe on medial surface

- slight lateral surface

239
Q

middle cerebral artery supplies what surface of the brain

A
  • most of the lateral surface
240
Q

border zone

A
  • aka watershed
  • region of brain receiving blood from two diff vessels (still right amt of blood)
  • lateral surface
241
Q

Small intestine overview

A
  • duodenum (25cm)
  • jejunum
  • illeum
  • surface area of tennis court
  • total length 3.5-6.5 meters
  • primary site of digestion and nutrient absorption
242
Q

Colon overview

A
  • absorption of water and electrolytes

- illeocecal valve opens to the cecum

243
Q

Haustra

A
  • folds of circular muscle that create sac-like segments along the colon
244
Q

GALT

A
  • GI associated Lymphoid tissue

- 25% the weight of the GI tract

245
Q

Diarrhea

A
  • 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
Q

Lactose Intolerance

A
  • 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
Q

Celiac Disease (Sprue)

A
  • 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
Q

Inflammatory Bowel Disease (IBD)

A
  • 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
Q

Hygiene hypothesis

A
  • 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
Q

Chronic Ulcerative Colitis

A
  • 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
Q

Toxic Megacolon

A
  • severe, rapid progression of Ulcerative Colitis`
252
Q

Crohn’s Disease

A
  • 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
Q

Presentation of Crohn’s disease

  • colon alone
  • illeocolic
  • scarring
A
  • colon alone: like UC
  • illeocolic: like apendicitis
  • scarring: like a bowel obstructio
254
Q

Diverticulosis

A
  • 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
Q

Diverticulitis

A
  • 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
Q

Bleeding with diverticulosis

A
  • small arteries rupture and lead to severe, painless, lower GI bleeding
  • blood thinners increase severity
  • other common cause is angiodysplasia: small vascular malformation
257
Q

polyp

A
  • mass that protrudes into the lumen of the gut
  • adenomatous polyps (adenomas) can progress to cancer
  • many others that don’t
258
Q

adenoma-carcinoma hypthesis

A
  • polyps accumulate a number of genetic mutations over time that lead to cancer
259
Q

colorectal cancer

A
  • 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
Q

Dukes staging system

A
  • A: tumors confined to bowel wall (muscular layer)
  • B: cancer extends beyond bowel wall
  • C: lymph node involvement
  • D: metastasis
261
Q

Family Cancer Syndromes GI

A
  • 20% due to direct genetic influence
  • Familial Adenomatous Polyposis (FAP; lynch syndrome)
  • Hereditary non-polyposis colon cancer
262
Q

Familial Adenomatous Polyposis (FAP) (Lynch Syndrome)

A
  • autsomal dominant
  • defect on chromosome 5
  • colon cancer inevitable by age 40
  • thousands of polyps develop
263
Q

Hereditary Non-polyposis Colon Cancer

A
  • patients with small numbers of polyps but clustering of colon, pancreas, ovar, and uterus cancers
  • defect in the mis-match repair gene
264
Q

Cerebrovascular Accident /Stroke

A
  • 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
Q

3 common patterns of injury with cerebrovascular accident

A
  • 73% infarcts (thromboembolisms, hypoxia, ischemia)
  • 19% intraparenchymal hemorrhages (secondary to hypertension)
  • 7% subarachnoid hemorrhages (rupture of aneurysms)
266
Q

what area of circulation most affected by hypertension?

A
  • border zone
267
Q

Arteriosclerosis vs Atherosclerosis vs Ateriolosclerosis

A
  • 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
Q

Hypoxia

A
  • decreased amount of oxygen in perfused tissue regardless of pressure
  • can lead to ischemia
269
Q

Ischemia

A
  • decrease in blood supply

- may be local or generalized

270
Q

Infarct

A
  • necrosis of tissue secondary to ischemia/hypoxia

- some strokes transient and reversible; don’t result in infarcts

271
Q

Cerebral emobli

A
  • 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
Q

Thrombosis

A
  • occlusion of vessel in situ

- secondary to formation of a blood clot in an already damaged artery by atherosclerosis

273
Q

Hemorrhage

A
  • usually associated with hypertension
274
Q

Blood-Brain Barrier

A
  • 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
Q

Infarcts

A
  • due to thrombosis, embolism, hypotension, or hypoxia

- small area of dead tissue

276
Q

transient ischemic attacks

A
  • loss of speech days or weeks prior to stroke
277
Q

Intraparenchymal hemorrhage

A
  • bleeding w/in brain parenchyma

- hypertensive hemorrhage most common cause

278
Q

subarachnoid hemorrhage

A
  • non-traumatic most commonly due to rupture of saccular aneurysm
279
Q

sacular/berry aneurysm

A
  • 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
Q

Brain Herniation

A
  • 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
Q

Parahippocampal/uncal herniation

A
  • entire part of parahippocampal gyrus herniates through the opening of the tentorium causing compression of the brainstem
  • followed by hemorrhage
282
Q

Cerebellar Tonsilar Herniation

A
  • 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
Q

Epidural Hemorrhage

A
  • 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
Q

Subdural Hemorrhage

A
  • 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
Q

why subdural hemorrhage in elderly

A
  • bridging veins very tight
286
Q

why subdural hemorrhage in young?

A
  • sign of child abuse

Path 404 (5 decks)

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