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Pathoma Flashcards

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1
Q

What CD receptor do neutrophils express

A

CD14

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2
Q

What role does PGI have

A

PGI = Platelet gathering inhibitor

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3
Q

What role do Mast Cells have

A

Release Histamine Vasodilation and increase vascular permeability

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4
Q

What is the second phase response of Mast Cells

A

Recruit Leukotrienes

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5
Q

4 Mediators that call in Neutrophils

A

LTB4, C5A, IL-8, bacteria products

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6
Q

Classical compliment system

A

(ig) GM makes Classic cars (C1)

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7
Q

Pathway/end result of compliment system

A

C3, C5, generation of membrane attack complex (MAC)

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8
Q

What components of compliment system trigger mast cell degranulation

A

C3a and C5a

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9
Q

one role of C5 in the compliment system

A

Calls in neutrophils

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10
Q

What does bradykinin do?

A

Same thing as histamine increase vasodilation, vascular permeability (++pain)

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11
Q

Prostaglandin E2

A

E2 fEEEEEver and pain

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12
Q

mediators that macrophages release

A

TNF-g, IL-1 Stimulate cox for PGE2 for fever

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13
Q

Leukocyte migration and rolling what are the binding factors

A

E-selectin, P-selectin Binds the Sialyl-Lewis

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14
Q

Leukocyte adhesion of vessel wall

A

ICAM (intercellular adhesion molecule)

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15
Q

Delayed separation of umbilical cord

A

Leukocyte adhesion deficiency (LAD) CD18

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16
Q

Lack of pus formation

A

Leukocyte adhesion Deficiency

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17
Q

Impaired phagolysosome formation

A

Chediak-Higashi

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18
Q

Whats the mechanism of O2 to HOCl (bleach) in a phagocyte degredation

A

O2 –> O2- –> H2O2 –> HOCL

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19
Q

What is the defect in Chronic Granuloma Dz (CGD) aka poor O2 dependent killing

A

Defect in NADPH

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20
Q

Maturation process of T cells. where they from and where do they go?

A

T cells are made in the bone marrow and mature in the thymus

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21
Q

Which T cells recognize which MHC class

A

CD4 t cells recognize MHC class 2 CD8 t cells recognize MHC class 1

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22
Q

CD4+ T cell activation requires what? (2 signals involved in activation) And what is their role

A

Antigen presenting cells (APCs) phagocytize antigen, process it, then present it on its MHC 2 membrane//B7 (on APC) binds to CD28 on MHC2 CD4 release cytokines to help in inflammation

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23
Q

What do CD4 helper T cells do?

A

They help both CD8+ / Bcells Broken into 2 subsets Th1 helps CD8 Th2 helps with B cells

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24
Q

Th1 helps what cells and how?

A

Th1 helps CD8 cells by releasing IL-2 (t cell growth factor and activator) and IFN-g (macrophages)

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25
Q

Th2 helps what cell and how

A

B cells IL-4 (class switching to gig and igE) IL-5 (Eosinophil chemotaxis and activation/maturation of B cells)

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26
Q

Whats a main enzyme that triggers apoptosis

A

caspase

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27
Q

B Lymphocyte maturation process

A

immature B cells are made in the bone marrow Undergo ig rearrangement to become naive B cells that express surface antigens IgM and IgD

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28
Q

B cell activation requires 2 signals

A

B cell presents antigen to CD4 via MHC 2 CD40 receptor (on Bcell) binds to CD40L on b cell

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29
Q

Marker for hematopoietic stem cell (in bone marrow)

A

Cd34

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30
Q

Stem cell of the lung

A

Type 2 pneumocytes

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31
Q

When converting type 3 collagen to type 1 collagen , which enzyme is used and what does it require as a cofactor

A

Collagenase Zinc

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32
Q

Tumor cell neoplasia is (monoclonal or polyclonal)

A

Monoclonal

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33
Q

3 things to think about when you see an enlarged lymph node

A

Metastatic cancer Reactive hyperplasia (simple infection) Lymphoma

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34
Q

What is a main cause of neuronal tube defects

A

folate deficiency

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35
Q

Anencephaly is associated with what involving the amniotic fluid

A

Polyhydramnios - too much amniotic fluid because the baby doesn’t have a developed brain to swallow it

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36
Q

Whats syringomyelia? and what brain malformation is associated with it

A

Degeneration of the spinal cord “CAPE/SHAWL-like” bilateral loss of pain and temp in upper extremities usually associated with Chiari malformation

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37
Q

Whats chiari malformation

A

herniation of the vermis through the foramen magnum

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38
Q

What is ALS (Amyotrophic Lateral Sclerosis)

A

Degenerative disorder of the upper and lower motor neurons (corticospinal tract) zinc copper superoxide dismutase mutation (SOD- removes free radicals)

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39
Q

Fredrick Ataxia

A

Degenerative disorder of the cerebellum Fred the FRAT star - mess up of Frataxin (iron binding protein) staggering and falling but has a sweet big heart diabets and hypertrophy cardiomyopathy GAA

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40
Q

What is the classic triad of meningitis

A

Stiff neck, headache, fever

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41
Q

How do you differentiate the etiology of meningitis when looking at the CSF via lumbar puncture

A

Bacterial- neutrophils with low CSF glucose Viral- lymphocytes with normal CSF glucose Fungal- lymphocytes with low CSF glucose

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42
Q

What happens in an epidural hematoma and what should you see on CT

A

fracture of the skull that severs the middle meningeal artery Lens shaped lesion on Ct

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43
Q

What happens in a subdural hematoma What should you see on CT

A

Rupture of the bridging veins Blood BENEATH the dura crescent shape

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44
Q

What is the key cell that myelinated axons in the CNS

A

Oligodendrocyte

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45
Q

What is the key cell that myelinated axons in the PNS

A

Schwann cell

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46
Q

What is multiple sclerosis

A

Autoimmune destruction of CNS myelin and oligodendrocytes HLA-DR2 SIIIN Scanning speech, intention tremor, incontinence, INO, Nystagmus

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47
Q

What is a lacunar stroke and which vessels do they most commonly involve

A

infarcts in the deep areas of the brain. Mostly in the lenticulostriate vessels off the MCA

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48
Q

Where does intracrebral hemorrhage mostly occur and why

A

in the basal ganglia due to the lenticulostriate vessels rupturing (micro aneurysms)

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49
Q

Worst headache of life

A

Subarachnoid hemorrhage usually rupture of saccular (berry) aneurysm usually located in the anterior circle of willis (ACA) Bloody or yellow CSF with tap Only blood at the bottom of the brain

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50
Q

What is Central pontine myelinolysis and how do you get it what is the major presenting case

A

Focal demyelination of the pons Caused by RAPID iv correction of Hyponatremia (from low to high the pons will die) Presents as Locked in syndrome- acute paralysis-

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51
Q

In GREY MATTER Degenerate neurons in the cortex? Degenerate neurons in the basal ganglia (deeper structure of the brain)?

A

Dementia Basal ganglia is required for movement so movement problems

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52
Q

Whats the most common disease for dementia? What is it? and grossly brain findings

A

Alzheimer’s dz (degeneration of the GREY matter in the cortex) Slow onset memory loss, disorientation, loss of learned motor skills Diffuse Brain atrophy, narrowing of Gyri/widening of sulk Neuritic plaques (amyloid precursor protein APP with ab amyloid) Neurofibrillary tangles (hyperphosphorylated tau protein)

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53
Q

What are risk factors for Alzheimer’s dz?

A

Deficient Ach ApoE2 (decreases risk) ApoE4 (increases risk) Presenillin -1/2 Neuritic plaques Amyloid precursor protein mess up that causes AB amyloid

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54
Q

What are neurofibrillary tangles, and in which dz are they seen?

A

Hyperphosphorylated Tau protein seen in Alzheimers Dz

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55
Q

Vascular Dementia

A

Dementia in elderly due to multiple infarcts of chronic ischemia

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56
Q

Pick’z DZ (Frontotemporal Dementia) it “picks” the frontotemporal

A

Frontal (behavioral) and Temporal (language) dementia Pick Bodies, ROUND Hyperphosphorylated tau

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57
Q

What is parkinson dz What are the clinical presentations (hint: its a a trap

A

Degenerative disorder of CNS involving dopamine deficiency neurons in the Substantia viagra Associated with Lewy Body (alpha-synuclein) Tremor (pill rolling) Rigidity (Cogwheel) Akinesia (brady) Posture (instability shuffle gait)

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58
Q

What are lewy bodies composed of? What disorder would you find these

A

composed of alpha-synuclein found in Parkinson Dz

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59
Q

Difference between lewy body dementia and Parkinson Dz

A

Lewybody dementia has early onset (parkinson takes a while) cortical lewy body= Ha’lew’cinations

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60
Q

What is the degeneration of gabarnergic (inhibitory) neurons in the brain? Where in the brain is the mess up? Whats the trinucleotide repeat

A

Huningtons Dz Caudate nucleus GABAnergic (inhibitory) neurons are destroyed CAG (has anticipation so it gets worse with each generation) CAG (C)audate loses (A)ch and (G)aba

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61
Q

What is the striatum and what composes it

A

Striatum is the basal ganglia which is important in movement. The caudate and the putamen makes it

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62
Q

What is Hydrocephalus and what TRIAD does it present? (wet whack and wobbly) and what usually improves it

A

Increased CSF resulting in dilated ventricles Urinary incontinence, dementia, gat instability (magnetic feet) Lumbar puncture (LP) relieves pressure

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63
Q

With hydrocephalus you should be thinking the stretching of the _______

A

corona radiata

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64
Q

Spongiform Encephalopathy

A

Degenerative dz of prion protein most common form is CJD

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65
Q

Creutzfield Jakob dz (CJD)

A

spongiform encephalopathy rapid dementia Ataxias and startle myoclonus

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66
Q

What is the role of the astrocytes?

A

Forms the blood brain barrier

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67
Q

What are the tumors that arise from astrocytes? kids/adult

A

Kids: Pilocytic Astrocytoma Adults: Glioblastoma Multiforme

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68
Q

What is the role of Oligodendrocytes?

A

Myelinate axons in the CNS

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69
Q

What are the tumors that arise from oligodendrocytes? Kids/adults

A

Kids: n/a Adults: oligodendroglioma

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70
Q

What is a glioblastoma multiforme? where does it arise

A

Malignant tumor of the astrocytes in brain Most common malignant CNS tumor in adults Crosses the Corpus callosum- buffterly glioblastoma Psuedopallisading GFAP

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71
Q

What is a meningioma what does it look like on histo?

A

Benign tumor of the arachnoid cells? Most common benign tumor “Whorl cells”

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72
Q

What is a Schwanomma? which cell type does it arise? What section of brain does it involve /histo

A

benign tumor of Schwann cells in the PNS Usually located at the cerebellar pontine angle (CPA) and messes with the Cranial Nerve CN8 s100+

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73
Q

Oligodendrogliomas / what cell it arises from / what section of the brain does it involve / histo

A

Arise from the oligodendrocytes in the white matter (bc they mylelinate-white) fucks with the frontal lobe fried egg appearance calcified tumor

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74
Q

What is the most common CNS Tumor in children and where does it arise (Remember that most kid CNS tumors are below the tentorium)

A

Pilocytic Astrocytoma Cerebellum Rosenthal fibers GFAP

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75
Q

Medulloblastoma /histo

A

CNS tumor in kids Neruoectodermal Tumor Former wright rosettes small blue cells

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76
Q

Which cells line the ventricular space in the brain

A

ependymal cells

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77
Q

ependymoma

A

Malignancy of the ependymal cells commonly arises in 4th ventricle hydrocephalus?

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78
Q

Craniopharygioma

A

tumor that arises from the remnants of the Rathe’s pouch (pituitary) compression of optic chiasm Bitemporal hemianopsia

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79
Q

What is Bitermporal Hemianopsia and what causes it

A

Compression of the optic chiasm that leads to loss of lateral vision

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80
Q

What is the most common form of vasculitis and who does it usually effect? what are some symptoms? Tx?

A

Temporal (giant cell) arteritis Granulomatous Vasculitis Older women Headache (temporal), visual disturbances (ophthalmic), jaw claudication Tx-corticosteroids

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81
Q

Takayasu Arteritis

A

Same as temporal arteritis (granulomatous vasculitis) But its usually in younger asain females (less than 40) “pulseless dz” Tx=corticosteroids

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82
Q

Polyarteritis Nodosa

A

Necrotizing vasculitis, involving most organs except the lungs usually a Serum Hep. B surface antigen String of pearls

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83
Q

Kawasaki Dz. What is it and who does it affect, and which artery does it mainly fuck up? How do you treat it

A

Vasculitis affecting asain children less than 4 yrs old. CRASH and Burn Conjunctival injection, Rash, Adenopathy, Strawberry tongue, Hand (foot) edema and fever Coronary Artery IV immunoglobulin and ASPIRIN

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84
Q

Buergers DZ what is it/ the main cause? and whats the clinical finding

A

Medium vessel vasculitis Caused by heavy smoking Autoamputation of digits

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85
Q

Wegener Granulomatosis We’C’ener Whats the tx

A

Small vessel vasculitis involves the C’s Nasopharynx/lungs/kidney Triad -necrotizing vasculitis, necrotizing granuloma in the lung/upper airway, necrotizing glomerulonephritis C-ANCA tx- Cyclophosphamide

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86
Q

Microscopic Polyangiitis? which organ does it affect? similar to which other small vessel vasculitis except for? how do you treat it?

A

Small vessel vasculitis affects lung and kidney no granulomas and no nasopharyngeal involvement Tx-Cyclophosphamide P-ANCA

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87
Q

Churg-Strauss? Which organ does it affect? Which small vasculitis is it similar to? how do they differ?

A

Small vessel vasculitis Necrotizing granulomatous vascuilits w/ eosinophils involves lungs and heart Similar to microscopic polyangiitis (Both have p-ANCA but differ bc it has granulomas and ASTHMA and no peripheral eosinophilia)

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88
Q

HSP (Henoch Schönlein Purpura)? what population is most common? whats the clinical presentation what infection does it usually follow

A

Small vessel vasculitis due to IgA immune complex deposition (IgA nephropathy) most common in children Palpable purpura on BUTT/LEGS Follows Upper Respiratory Infection

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89
Q

What is the defined limits of Hypertension and risk factors

A

BP >140/90 age,race, obesity, high salt diet

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90
Q

What is atherosclerosis? which size vessels does it effect? what are the 4 main arteries it hits (in order of occurrence) how much occlusion do you need to have symptoms

A

A buildup of cholesterol plaque in medium/large muscular arteries Abdominal Aorta > coronary a.> popliteal A. > carotid greater than 70%

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91
Q

What is the progression of Atherosclerosis

A
  1. endothelial cell fuck up 2. macrophage and LDL accumulation 3.Foam cell formation 4. Fatty streaks 5. Fibrous plaque
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92
Q

What are the two types of ArteriOLOsclerosis

A

Hyaline:Vascular thickening of vessel wall with protein caused by Hypertension and diabetes Hyperplastic: Onion Skinning caused by sever HTN

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93
Q

What causes Hyaline ArteriOLOsclerosis What does it lead to?

A

HTN and Diabetes HTN increased BP forces protein into the vessel wall Diabetes- Causes vessel wall to be leaky so protein leaks in leads to ischemia and glomerular scarring

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94
Q

What causes Hyperplastic AteriOLOsclerosis

A

Thickening of vessel wall due to hyperplasia of smooth muscle due to malignant HTN

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95
Q

Where do you see fibrinoid necrosis (beads on string)

A

Malignant HTN

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96
Q

Whats an Aortic Dissection What disorders are prone for Dissections Most common Cause of death

A

When a rip in the INTIMA of a vessel causes blood to penetrate and create a lumen between intima and media Literally rips through and dissects the two layers due to Pre-existing weakens of the media (HTN) Connective tissue disorders (Marfan Syndrome) Cardiac tamponade

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97
Q

Thoracic Aneurysm What dz most commonly leads to it whats the most common clinical presentatoin

A

Balloon like dilation of the aorta. must have weakness in the wall Tertiary syphilis - caused by endarteritis of vaso casorum (prevents nutrients to the wall of vessels so it atrophies) Pulsatile abdominal mass

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98
Q

Chest pain that arises with exertion or stress is ____ What dz commonly leads to it Whats the most common presentatoin

A

Stable angina

atherosclerosis- not enough blood getting to the heart so it becomes hypoxic/ischemic

Chest pain that radiates to left arm or jaw -St depression Tx- rest or Nitroglycerin

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99
Q

Chest pain that occurs at rest is ____ What causes it? Tx?

A

Unstable angina Rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of the coronary artery -Nitroglycerin high risk of MI

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100
Q

Vasospasm of the coronary artery? Tx

A

Prinzmetal angina tx-CCB’s or Nitrates

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101
Q

Difference between myocardial infarct (MI) and unstable angina

A

MI has Thrombosis of a Plaque with COMPLE occlusion. also has IRREVERSIBLE damage to myocytes

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102
Q

Which chamber of the Heart does MI mostly occur? Which coronary artery usually gets occluded

A

LEFT VENTRICLE 1-Left anterior descending (LAD) anterior wall and atrial septum necrosis 2. Right coronary artery-poserior wall of heart

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103
Q

ST elevation MI (STEMI) What type of infarct thickness?

A

Transmural Full thickness

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104
Q

non ST elevation MI (NSTEMI) thickness?

A

subendocardial infarcts

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105
Q

Which enzymes are indicative of an MI

A

TROPONIN rises at 2-4hrs peaks at 24 hrs elevated for a week CK-MB rises and goes down quickly can be used to determine multiple infarcts

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106
Q

Which cardiac enzyme is used to determine multiple infarcts

A

CK-MB because it rises and galls quicker than TROPONIN

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107
Q

Tx for Myocardial infarction

A

Aspirin/Heparin (to prevent further clotting) Supp. O2 Nitroglycerin Beta Blockers

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108
Q

What is the progression of an MI (days weeks months)

A

1 day / 1 week / 1 month coagulative necrosis (dead cells) / Neutrophils and macrophages / granulation tissue and scar

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109
Q

Type of pericarditis that occurs 6 weeks after an infarct due to autoantibodies against the pericardium

A

Dresslers Syndrome

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110
Q

Whats congestive heart failure mainstay treatment?

A

When the heart fails to pump appropriately (usually backs into the lungs) Tx-ace inhibitors

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111
Q

Hemosiderin-laden macrophages

A

Heart failure cells found in lungs with pulmonary edema

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112
Q

Whats the most common congenital heart defect and what syndrome is it associated with

A

Ventricular septal defect (VSD) associated with FETAL ALCOHOL SYNDROME

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113
Q

What is the mnemonic for left to right shunt yes right to left?

A

(R)ight to (L)eft shunts are eaRLy cyanosis (L)eft to (R)ight occur LateR cyanosis

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114
Q

What is atrial septum defect? what defect causes this

A

defect in the septum between atriums Osmium secundum defects

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115
Q

Holocystolic machine like murmur cyanosis of lower extremities How do you treat this What disorder is it associated with

A

Patent ductus arteriousus PDA failure of ductus arterioles to close cyanosis of lower extremities Tx-ENDomethacin ends PDA Congenital rubella

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116
Q

Tetralogy of Fallot

A

R–>L shunt most common cause of eaRLy cyanosis (fixed with squatting) Pulmonary stenosis Boot shaped heart (hypertrophy) Overriding aorta/VSD

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117
Q

Transposition of the Great vessels? What dz is it associated with

A

Failure of the aorticopulmonary system to spiral (they swap places) Maternal diabets

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118
Q

What is rheumatic fever? What is it usually caused by?

A

occurs 2-3 weeks after strep throat (alpha-beta hemolytic streptococci) M- protein JONES criteria which is joints, heart problems, nodules, erythema marginatum, s-chorea arthritis, pan(all layers)carditis (mitral valve), subQ nodules, rash, rapid movement

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119
Q

Jones criteria whats it used to diagnosis

A

joints, heart problems, nodules, erythema marginatum, s-chorea arthritis, myocarditis (mitral valve), subQ nodules, rash, rapid movement

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120
Q

Aortic Valve Stenosis how do you get it? What cardiopathy and other symptoms does it lead to?

A

Narrowing of the aortic valve Systolic ejection click followed by crescendo- decrescendo murmur “wear and tear of valve” -presents in late adult hood or when you have a bicuspid valve instead of (tri) leads to Left ventricular hypertrophy SAD Scope, Angina, and Dyspnea on exertion

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121
Q

Aortic Regurgitation why does it happen?

A

“blowing murmur” Back flow of blood from aorta into LV during diastole Aortic root DILATION or valve problems Hyperdynamic circulation (bounding pulse, pulsating nail bed, head bobbing)

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122
Q

What is hyper dynamic circulation and what causes it?

A

Seen in aortic regurgitation Bounding pulse, pulsating nail bed, head bobbing the regurg increases the volume of the next stroke in LV so it keeps adding and adding pressure

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123
Q

Mitral valve prolapse

A

ballooning of the mitral valve into left atrium during systole Myxoid degeneration of the valve (floppy) *mid systolic click* like a parachute

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124
Q

Mitral Stenosis what happens to the atrium

A

Narrowing of the mitral valve, usually due to rheumatic valve dz Opening snap followed by a rumble LA overload- pulmonary congestion (edema)

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125
Q

Which organism causes Endocarditis (low virulence)

A

S viridians most common cause of endocarditis, infects previously damaged valves results in small vegetations that don’t destroy valves

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126
Q

Which organism is the most common cause of (acute) Endocarditis in IV drug users and which valve is involved

A

S. Aureus (acute) Large vegetations on normal valves Most commonly Tricuspid

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127
Q

Which organism causes Endocarditis of prosthetic valves?

A

S. Epidermidis

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128
Q

Which organism causes Endocarditis with underlying colorectal cancer

A

S. Bovis

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129
Q

Endocarditis with Negative Blood cultures

A

HACEK Haemophilus, actinobacilus(aggregatibacter, Cardiobacterium, Eikenella, Kingella)

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130
Q

Clinical features of endocarditis

A

Fever, murmur, Janeway lesions(painless on palm or sole), Osler (ouch) nodes (painful on fingers or toes)

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131
Q

endocarditis with nodules on both sides of the valve And what is it associated with

A

Libman-Sacks Endocarditis SLE mitral valve

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132
Q

Dilated Cardiomyopathy (most common cardiomyopathy) What causes it tx-

A

Dilation of all 4 chambers systolic dysfunction (dilated so it can’t contract properly), valve regurgitation ABCCCD + p alcohol abuse, Beri beri, COXSACKE, cocaine use, Chagas, Doxorubicin toxicity and pregnancy Transplant

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133
Q

Hypertrophic Cardiomyopathy whats a huge problem with this

A

Hypertrophy of left ventricle commonly due to genetic mutations in Sarcomere protein Decreased cardiac output due to the heart being so tight. (it can’t dilate to get blood in) Can lead to SUDDEN DEATH due to ventricular arrhythmia myofibrillar disarray

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134
Q

Restrictive cardiomyopathy what are the causes

A

Decreased compliance of ventricles (won’t dilate so you have a diastolic problems sarcoidosis, fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), hematochromatosis LOFFLER SYNDROME- endomyocardial fibrosis with a prominent eosinophilic infiltrate

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135
Q

Loffler syndrome and does it lead to

A

endomyocardial fibrosis with a prominent eosinophilic infiltrate leads to restrictive cardiomyopathy

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136
Q

Myxomas were does it usually occur (which valve)

A

Most common primary cardiac tumor in ADULTS Usually occurs in the left atrium and causes syncope described as “Ball valve” obstruction

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137
Q

Rhabdomyoma

A

most common primary cardiac tumor in CHILDREN associated with tuberous sclerosis

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138
Q

what is primary hemostasis

A

injury to a blood vessel that results in a PLATELET PLUG (stabilized by secondary hemostasis)

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139
Q

What is secondary hemostasis

A

Stabilization of the platelet plug via coagulation cascade

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140
Q

Steps of thrombogenisis

A

1)Endothelial damage= vasoconstriction 2)Exposure: vWF is exposed to collagen and binds 3)Adhesion: Platelets bind to vWF via Gp1b (conformational change) platelets release ADP and Thromboxane 4a)ADP helps platelets adhere to endothelium via increased Gp2b/3a receptors 4b)platelet aggregation via FIBRINOGEN between Gp2b/3a receptors

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141
Q

Where does vWF come from?

A

Weibel-palade bodies of the endothelial cells and Alpha-granules of platelets

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142
Q

Clinical signs of Primary hemostasis fuck up

A

Mucosal and skin bleeding (nose -EPISTAXIS-, gi, menstrual)) bruising, petechia, purpura

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143
Q

Idiopathic Thrombocytopenia Purpura (ITP) what clinical values will you see Tx?

A

Autoimmune production of IgG antibodies against platelet antigens low platelet count, increased megakaryocytic tx-corticosteroids, ivig (the spleen produces the antibodies and also destroys them. so ivig will distract the spleen to give the bodys platelets a chance to recover), splenectomy

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144
Q

Microangiopathic hemolytic anemia

A

Small blood vessels get a platelet thrombus that shears any passing RBCs Shcistocytes (helmet cells)

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145
Q

Thrombotic thrombocytopenia purpura (TTP) tx=

A

platelet aggregation that leads to thrombocytopenia (purport from lack of platelets) Deficiency of ADAMTS13 (which breaks down vWF) so you have to much vWF which leads to increased platelet aggregation tx-plasmapharesis, steroids

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146
Q

Hemolytic-uremic syndrome

A

Thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure seen in children after Etec infection caused by Shiga like toxin

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147
Q

Bernard-Soulier syndrome? whats the defect in?

A

a defect in platelet plug formation due to decrease in Gp1b defect in platelet-to-vWF adhesion increase bleeding time

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148
Q

Glanzmann Thrombasthenia

A

genetic deficiency in Gp2b/3a platelet aggregation is impaired ( G2pb/3a is what connects platelet to platelet via fibrinogen

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149
Q

vWF disease tx-

A

deficient in vWF tx- desmopressin

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150
Q

Vit. K deficiencey

A

Decrease in synthesis of factors 2,7,9,10,C,S 7 having the shortest half-life

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151
Q

Warfarin

A

inhibits vit K synthesis via inhabiting epoxide reductase

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152
Q

Heparin induced Thrombocytopenia (HIT)

A

when you develop IgG antibodies against Heparin-bound platelet factor 4 (PF4) the antibodies activate platelets–> thrombosis and thrombocytopenia elsewhere

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153
Q

Disseminated inter vascular coagulation (DIC) whats the best screening test?

A

Secondary to other dz pathologic activation of coagulation cascade widespread micro thrombi that leads to ischemia and infarction Consumption of all these platelets leads to bleeding everywhere else (especially IV and mucosal sites) test- Elevated D dimers (when you split fibrin it produces D dimers)

154
Q

What blocks activation of plasminogen

A

Aminocaproic acid

155
Q

What two characteristics would you see in a thrombosis

A

Lines of zahn attachment to vessel wall

156
Q

Vitamin B12 or folate deficiency leads to elevated ________

A

homocysteine levels

157
Q

TetrahydroFOLATE to methionine

A

THF–> gives off methyl to Vit. B12—> gives methyl to Homocysteine —-> methionine

158
Q

Whats the role of Protein C or S

A

Inactivate factors V and VIII in coag cascade

159
Q

whats the deal with factor V leiden

A

Resistant to degradation/inactivation by Protein C

160
Q

Whats are the anemia subtypes (based off of MCV) mean corpuscular volume (size of red blood cell)

A

Microcytic MCV 100

161
Q

Role of ferroportin Role of Transferrin Role of Ferritin

A

Transfers iron into the blood Delivers iron to liver and bone marrow macrophages Iron Storage

162
Q

Why do you get anemia of chronic dz?

A

With chronic dz, you get prolonged inflammation. and in order to stop whatever is causing the sickness, the body increases hepcidin (which fucks up ferroportin and prevents release of iron from ferritin ) which decreases iron transport —-> iron deficiency —> anemia ferritin goes up/ TIBC goes down Serum iron goes down

163
Q

What does hepcidin do

A

Prevents release of iron from storage sites to deprive any infection of iron and kill it off

164
Q

Sideroblastic anemia

what are some of the causes

Tx?

A

Defect in protoporphyrin synthesis –> defect in Hb. due to X-linked defect in ALA synthase

defect in protoporphyrin leads to iron getting trapped in mitochondria of erythroblasts

congenitcal (ALA synthase), lead poisoning, alcoholism, or B6 Deficiency (pyridoxine)

tx-B6 pyridoxine

165
Q

what attaches Protoporphyrin to Iron (to make heme)

where does this happen

A

Ferrochelatase

in mitochondria

166
Q

Ringed sideroblasts

A

when protoporhyin synthesis is messed up so iron gets loaded into mitochondria.

This iron has nothing to bind to so its trapped there. These iron-laden mitochondrias form rings around the nucleus

167
Q

Thalassemia

A

Decrease in synthesis of Globulin chains

(leads to microctyic anemia)

168
Q

alpha Thalassemia

4 allele deletion

3 allele deletion

2 and 1 allele deletion

A

Normally you have 4 alpha alleles

Defect in A-globin deletion

4 allele-no alpha globin, excess gamma globin, (makes gamma4 -Hb Barts) Hydrops fetalis

3 allele- very little alpha globin, Excess ß-globin (HbH)

2/1 not clinicilaly severe

169
Q

whats the significance of cis vs trans deletions in alpha-thalassemia

A

cis is when 2 alpha alleles are knocked out on the same chromosome. this can lead to to severe thalasemia in offspring (Prevalent in Asains)

Trans isnt that bad (African population)

170
Q

ß-Thalassemia (2 beta genes)

Minor (ß/ß+) (normal/diminished)

Major (ß°/ß°) both B are wiped out

A

Gene mutation

minor-asymptomatic with Increase in HbA2

major

Absent Beta chain, target cells,

massive erythroid hyperplasia- expansion of hematopoiesis into marrow of Skull and facial bones (crew cut and chipmunk like face)

extramedulary hematopoiesis- liver and spleen starts to make it (hepatosplenomegaly)

Risk of Parvovirus B19- aplastic crisis

2° hemochromatosis

171
Q

Macrocytic Anemia

(Megaloblastic anemia)

MCV? what deficiencies cause it? why do the deficiencies lead to it

A

MCV>100

Folate or Vit. B12 deficiency

(1 less division so theyre macro) due to mess up of DNA precursors

Hypersegmented Neutrophils

172
Q

whats the role of folate and Vit B12 in synthesis of DNA (flow chart)

A

Tetrahydrofolate has a methyl and in order for it to make DNA it has to give that methyl to Vit. B 12

Vit B12 then gives that methyl to Homocystiene.

Homocystiene + methyl = Methionine

173
Q

Folate

Where is folate absorbed?

what casuses its deficiency

Clinical findings of deficiency

Lab findings

A
  • In the Jejunum
  • Poor Diet (alcoholics,elderly), Increased demand (preggos, cancer, hemolytic anemia), Drugs methotrexate
  • Megaloblastic anemia (macrocytic RBCs, Hypersegmented Neutrophils), Glossitis
  • Decreased serum folate(duh),
  • Increased* Homocysteine( piles up because folate doesnt pass Methyl to vit.b12 –>so vit b12 cant change homocysteine to methionine

Methylmalonic acid is Normal

174
Q

Vit. B12 (Cobalamin)

How is it absorbed/where

What causes its deficiency (alot)

Clinical and lab findings

A

First needs to be cleaved by pancreatic enzymes

Then, it binds to Intrinsic Factor (IF) to be absorbed in the Ileum. Large hepatic stores so it takes a long time to develop deficiency.

-caused by insufficient uptake (Vegan), malabsorption (Crohn dz), Pernicious anemia (Autoimmune destruction of parietal cells- cant make IF)

Diphyllobothrium Latum (fish tapeworm)

  • Macrocytic anemia with Hypersegmented neutrophils, Glossitis
  • Subacute Combined Degeneration of Spinal Cord -B12 converts methylmalonic acid –> Succinyl Coa. so without B12 you get a shit tone of mma which is toxic to myelin
175
Q

Pernicious Anemia

A

Autoimmune destruction of Parietal cells.

This leads to a deficiency of Intrinsic Factor (IF)

Which means you cant absorb Vit B12

176
Q

What are the 2 major processes that Vit B12 are invovled in?

A
  • In the synthesis of DNA, by accepting methyl from Tetrahydrofolate, then giving it to Homocysteine
  • Converts Methylmalonic acid —-> Succinyl CoA myelin synthesis

too much methylmalonic acid is toxic to myelin

177
Q

Normocytic Anemia

MCV?

what does the reticulocyte count look like?

A
  • MCV 80-100
  • Increased reticulocyte count/percentage (falsely elevated) due to destruction of RBCs

You must correct it tho.

178
Q

In normocytic anemia, what are the perameters for when you correct the reticulocyte count?

Whats the equation

A

>3% indicates good response by bone marrow; suggests peripheral destruction

<3% indicates bad response by bone marrow; suggests underprodcution

Reticulocyte count x (Hematocrit/45)

in the example it would be a bone marrow problem

179
Q

Extravascular hemolysis

Which Anemia does it cause

What are clinical findings

A
  • Normocytic anemia
  • Extravascular destuction occurs from macrophages in spleen
  • Anemia with Splenomegaly, Jaundice due to unconjugated bilirubin (increased risk for gallstones), marrow hyperplasia with corrected reticulocount >3%

remember that when hemoglobin is broken down, the protoporhyrin of heme gets turned into Unconjugated billirubin

180
Q

Intravascular Hemolysis

What type of anemia does it cause

lab findings

A
  • Normocytic Anemia
  • Destruction of Hemoglobin in the blood vessel. Haptoglobin (binds to free Hb and brings it back to spleen)

Hemoglobinemia, Hemoglobinuria, Hemosiderinuria

181
Q

Haptoglobin

A

Binds free hemoglobin (Hb) and brings it back to spleen.

levels of haptoglobin are decreased in intravascular hemolysis bc they get used up

182
Q

Hereditary Spherocytosis

clinical findings

how is it diagnosed

tx?

A

Extravascular hemolysis due to defect in RBC membrane (ankyrin, band 3, spectrin are protein fuckups)

Small round RBC with no central pallor (premature removal by spleen)

Increased MCHC (mean corpuscular hemoglobin concentration) only dz with this

  • Splenomegaly, Aplastic crisis (ParvoVirus B19 infection)
  • osmotic fragility test
  • Splenectomy
183
Q

Sickle Cell Anemia

whats the mutation?

what causes the sickling

What protects against the sickling (tx)

clinical findings

A

Auto Recesive mutation in the ß gene (glutamic acid with valine)

  • Stressors such as Low O2, high altitude, acidosis, dehydration
  • HbF(fetal), give hydroxyurea to increase HbF

‘-Aplastic crisis (parvovirus B19),

Painful crisis: dactylitis (sausage fingers), acute chest syndrome, avascular necrosis

Autosplenectomy (howell jolly bodies)- due to infarct of the spleen. increases risk of infection S. pneumonia

Salmonella osteomylitis

184
Q

Hemoglobin C

whats the mutation

A

Auto Recessive mutation in ß Chain

Glutamic acid is replaced by Lysine

185
Q

Paroxysmal nocturnal hemoglobinuria (PNH)

why does it happen?

lab findings

what does it lead to

Tx

A

aquired dsyfunciton of GPI via hematopoietic stem cell

(anchors decay-accelerating factor -DAF CD55- that protects RBC from complement activation)

at night we breath slower leading to respiratory acidosis –> activation of compliment (intravascular hemolysis) which will fuck up these RBCs since theyre predisposed already

  • hemoglobinemia, hemoglobinuria
  • leads hemolytic anemia (duh), pancytopenia, thrombosis

10% of pts develops AML

-tx eculizumab (compliment inactivator)

186
Q

G6PD deficiency

whats its function

what causes oxidative stres

what cells does this produce?

Clinical signs

A

X-linked Recessive d.o –>reduced half life of G6PD

(increases RBCs succeptible to oxidative stress)

G6PD helps create NADPH. NADPH helps produce glutathione which protects against oxidative stress

-Infections, Fava Beans

Heinz bodies & Bite cells

Back Pain from all the released Hb(nephrotoxic)

187
Q

Immune hemolytic Anemia

What are the different types

what are they associated with

A

Warm IgG: EXTRAVASCULAR chronic anemia due to IgG binding to RBC and removing membrane (results in spherocytes). Associated with SLE and CLL (Methyldopa) / (Warm weather is GREAT)

Cold IgM: Acute anemia triggered by cold. Associated with CLL, Mycoplasma pneumonia, Infectious Myonucleosis. (Cold weather is MMMiserable)

188
Q

What is the Coombs test?

Direct. vs indirect

A

direct- do i have cells already bound by IgG? you give them anti- IgG. so if the answer is yes, the RBCs wil agglutinate and percepitate

Indirect- Does the pt have antibodies in their serum? normal RBCs added to patients serum. if serum has the antibodies, the RBCs agglutinate when Coombs is added

189
Q

Whats the CD for hematopoeitic stem cells?

Give the lineage of everything that it can produce

A

CD34

190
Q

What are some causes of Neutropenia

A

Sepsis/severe infection

Drugs (chemotherapy)

191
Q

What are causes of Lymphopenia

A

Immunodeficiency: HIV, SCID, SLE, sepsis

High levels of cortisol (or corticosteroids)-these cause apoptosis

Radiation (lmyphocytes die quickest)

192
Q

Whats the anatomy of lymph node

What areas are the B and T cells located

A

B cells are in the cortex (follicles)

T cells are the in the Paracortex (swells with viral infection)

193
Q

What are the markers for Lymphoblasts in the blood?

Myeloblasts?

A

TdT+ (marker of pre T and pre B)

CD10,19, 20 (marker of pre B)

_______________________

myeloperoxidase(+)

Auer Rod

194
Q

Tell me about ALL (acute lymphoblastic Leukemia)

whats the good translocation

A

Most frequently in childeren

Highly associated with Down syndrome (after age of 5)

T(12;21) has good prognosis

Subdivided into T-ALL and B-ALL

**acute is always immature

195
Q

T-ALL what physical finding should give it away

A

T should make you think of Thymic (Mediastinal mass)

196
Q

AML (Acute Myeloblastic leukemia)

whats the classic translocation (also known as APL-acute promyelocytic leukemia). and what does this trans do?

what systemic problem can AML lead to? and how do you treat it?

A

Myeloperoxidase (+) ->these aggregate to form Auer Rods

APL- T(15;17) fucks up the retinoic acid receptor ->the cells cant mature

can lead to DIC (treat with ATRA-causes blasts to mature)

197
Q

under AML, if the leukemia is specifically monocytes, what should you think of

speciffically megakaryocytes

A

lack Myeloperoxidase//heavily infiltrates the Gums

Associated with Downs syndrome before 5

198
Q

whats the deal with CLL

who does it affect, what are the cell markers

what type of cells will histo show

what can CLL transform into?

A

Usually in older adults

proliferation of naive B cells (CD5,20)

smudge cell

Diffuse Large B-cell Lymphoma (DLBCL)

199
Q

Hairy Cell Leukemia

what does it stain positive for?

clinical features

A

proliferation of Mature B-cells

hairy/fuzzy cells

stains positive for TRAp

massive Splenomegaly (red pulp) / dry tap on bone marrow aspiration

200
Q

CML (chronic myelogenous leukemia)

whats the translocation

how do you treat it

what can it transform to?

A

increase of mature granulocyte (mostly basophils) LAP (-)

Philadelphia chromosome t(9;22)

BCR-ABL (increases tyrosine kinase activity)

To treat, you gotta inhibit tyrosine kinase - Imatinib

can transform into Acute Leukemia

201
Q

Polycythemia Vera

what is messed up(mutation) that causes it

clinical symptoms

Treatment?

A

proliferation of mature myeloid cells (especially RBCs) EPO is decreased

JAK2 kinase mutaiton

-blurry vision, Increased risk of thrombosis (Budd chiari), flushed face, itching after bathing (mast cells release histamine)

tx-phlebotomy (get rid of some of that blood)

2nd tx is hydroxyurea

202
Q

2° Polycythemia (reactive)

A

Increased EPO from either lung dz (low O2)

or Tumor that produces EPO (renal cell carcinoma)

203
Q

Essential Thrombocythemia

A

proliferative disorder of myeloids (specifically Platelets)

shit ton of platelets - either bleeding or thrombosis from lack of function or overfunctioning platelets

204
Q

Myelofibrosis

what does it lead to

what cells does it make

A

myeloproliferative disorder (specifically Megakaryocytes)

JAK2 kinase mutation

marrow fibrosis - so the marrow cant make new RBCs which means you get extramedullat hematopoeisis in the spleen (splenomegaly)

Teardrop cell

205
Q

Lymphoma

What are the subcategories

A

Tumor that arises from lymphocyte

Hodgkin lymphoma &

Non-Hodgkin Lym : Burkitt, DLBCL, Mantle,

206
Q

Follicular Lymphoma

what is it/clinical signs

translocation

A

NHL

neoplastic Bcells (CD20) that make small follicle like nodules

Painless LAD (waxing and waning)

T(14;18) - switches heavy chain IG with BCL-2 (inhibits apoptosis) so you get over exp resion of BCL-2

207
Q

What does BCL-2 do

A

cell marker that inhibits apoptosis

208
Q

Mantle Cell Lymphoma

whats the translocation

A

neoplastic B cells that expand the mantle zone

t(11;14) cyclin D and IG Heavy chain

overexpression of cyclin D causes cell to go from G1 to S phase

209
Q

What does Cyclin D do?

A

causes cell to go from G1 to S phase in cell cycle

210
Q

Burkitts Lymphoma

What is it associated with

what are the 2 different forms

Translocation/ what does histo look like

A

neoplastic B cell prolif (CD20)

associated with EBV

-Endemic African: Jaw lesion // Sporadic: abdomen

t(8;14) : C-myc (promotes cell growth)

Starry Sky Appearance

211
Q

Diffuse Large B-cell Lymphoma (DLBCL)

A

most common form of NHL

large nodes or extranodal mass

212
Q

Hodgkin Lymphoma

what cell do you see on histo

A

Reed-sternberg cells (owl eyes) CD15/30

you get B-symptoms: fever, night sweats, weight loss

213
Q

Multiple Myeloma

what are some sypmtoms (CRAB)

which IG’s are most spiked

associated with

A

Malignant proliferation of plasma cells in marrow

Fried egg appearance

HyperCalcemia, Renal involvment, Anemia, Bone lesion (lytic- punched out)

M Protein spike (increase in Monoclonal immunoglobin (IG G/A)

Increased risk of infection, Rouleaux formation (stacked RBCs), Ig light chains in urine

214
Q

Monoclonal gammaopathy of undetermined significance (MGUS)

Waldenstrom macroglobulinemia

A

When you get an M spike but you dont have any of the CRAB symptoms of Multiple Myeloma

M spike of IgM with no CRAB. hyperviscosity syndrome like blurred vision and raynaud

215
Q

Langerhan cell Histiocytosis

what would histo show

clinical signs?

A

proliferative disorder of (langerhan )dendritic cells found in skin. cells express s100

  • Birbeck granules (Tennis racket)
  • skin rash/ lytic bone lesion
216
Q

what artery does horse shoe kidneys get stuck on?

A

inferior mesenteric artery

217
Q

PKD

A

inherited defect

Bilateral Enlarged kidneys due to cysts in renal cortex and medulla

218
Q

Autosomal Recessive PKD

what are the clinical signs

A

usually presents in infants.

Renal failure, HTN, Hepatic fibrosis

Potters Syndrome

219
Q

Autosomal Dominant PKD

ADPKD (ADult)

where is the mutation?

How do they present?

What other d.o’s are they associated with?

A

The mutation is in PKD1(85%) or PKD2

  • present with Flank pain, hematuria, HTN, Renal failure(Duh)
  • Berry aneurysm, hepatic cysts, mitral valve prolapse

(cysts in the liver, brain, and kidney)

220
Q

Medullary cystic Kidney Dz

what will the kidneys look like?

A

inherited defect of Cysts in the collecting ducts

Shrunken Kidneys

221
Q

Azotemia

A

Increase in urine BUN and Creatinine

222
Q

Acute Renal Failure

A

Abrupt decline in renal function measured by Azotemia (Increase in BUN and Creatinine

223
Q

Pre-renal azotemia

Intra-renal failur

Post-real Azotemia

A
  • Decrease in Renal BLood Flow
  • -*Acute Tubular Necrosis
  • -*Outflow Obstruction
224
Q

Pre-renal azotemia

A
  • Due to decrease in Renal blood flow (Hypotension)
  • Increased BUN/Creatinine Ratio

(BUN is absorbed, creatinine is not)

Hypotension so the kidney is tryna hold onto whatever it can to conserve volume

BUN/Creatinine ration >20

225
Q

Acute Tubular Necrosis

(intra renal failure)

Whats seen in the urine casts?

what are serum and lab findings

What are the two ways to get it?

A

Injury and necrosis of Tubular epithelial cells. These necrotic cells plug the tubule which obstructs and Decreases GFR

  • Muddy brown casts
  • bc the epithelial cells are fucked you get messed up (decreased) resorption of:

BUN which means BUN:CR is <15

Na which means FeNA >2%

Inability to concentrate urine — Osmalitly<200

-Ischemic & Neprotoxic

226
Q

Ischemic Acute Tubular Necrosis (ATN)

which parts are most often fucked up

A

Decreased Blood supply results in necrosis of tubules

-PCT(proximal tubule) and Thick ascneding limb

227
Q

Nephrotoxic Acute Tubular Necrosis (ATN)

What parts get fucked up?

what agents are nephrotoxic?

A

Necrosis of tubule cells due to toxic agents

  • only PCT (proximal tubule)
  • Aminoglycosides, heavy metals, Myoglobinuria (Crush injury), Ethylne Glycol, Radio contrast
228
Q

Acute Interstitial Neprhitis

which drugs cause this?

what is a giveaway if you see it in the urine

what can it lead to?

A

Intra renal ARF (acute renal failure)

Drug induced hypersensitivity reaction

  • NSAIDs, Penicillins, Diuretics
  • Eosinophils in the urine
  • can lead to Renal Papillary Necrosis
229
Q

Renal Papillary Necrosis

  • clinical symptoms
  • causes (SAAD Papa)
A

Necrosis of Renal papillae

Gross Hematuria and flank pain

-causes: Sickle cell, Acute pyleonephritis, Analgesics(Nsaids), Diabetes Mellitus

230
Q

NephrOtic Syndrome

Whats the main hallmark of this?

what all lost becasue of it

List all 6 dz that leads to this

A
  • PrOteinuria (>3.5g/day). due to any damage of the GFR barrier

Loss of Albumin* which causes *EDEMA

Loss of immunoglobulins –> increased infections

Loss of Antithrombin III(ATIII) –> Hypercoag

Hyperlipidemia- frothy urine

  • Minimal Change Dz, Focal segmental glomerulosclerosis (effacement of podocytes)
  • Membranous Nephropathy, MPGN (deposition of immune complexes)
  • Diabetic Glomerulonephropathy, Amyloidosis
231
Q

Minimal Change Dz (MCD)

who gets it

what causes this which can be seen on EM

which protein do you lose?

treatment?

A

most common cause of NephrOtic syndrome in kids

-effacement of foot processess (podocytes) due to cytokines

you only lose albumin

-tx: Steroids

232
Q

Focal Segmental Glomerulosclerosis

Who usually gets this?

What is it associated with

what what it look like on histo

whats special about the treatment and what can it progress to

A
  • most common cause of NephrOtic syndrome in Hispanics and Blacks
  • HIV, Heroine, and Sickle cell
  • -*Focal (not all glomeruli) Segmental (only part of affected glomeruli) Slcerosis (deposition of pink collagen)
  • poor response to steriods and can progress to chronic renal failure
233
Q

Membranous nephropathy

who gets it

whats it associated with

whats it look like on histo due to?

A

Most common cause of NephrOtic syndrome in Caucasian adults

-Hep B/C, Solid Tumors, SLE

Very thick membranes due to immune complex depositions

-Spike and Dome on EM

234
Q

Membrano-Proliferative Glomerulonephritis

what does it look like on stain

divided into two types. explain them and what they are associated with

A

Thickening of the glomerular membrane due to deposits of Immune complexes

Tram Track appearance because the membrane gets split by the mesangial cells

  • Type 1: Subendothelial deposits. Hep B/C
  • Type 2: Basement Membrane deposits. C3 Nephritic factor (activates complement by stablizing C3 convertase)
235
Q

Where are the immune deposits in MPGN (membranous proliferative glomerulonephritis) and Membranous nephropathy

A

MPGN type 1: Subendothelia

MPGN type 2: basement membrane

Membranous: subepithelial

236
Q

Diabetic Glomerulonephropathy

What does the diabetes do? how to treat it

what kind of nodules will you see?

A

cause of NephrOtic syndrome

High blood sugar leads to Nonezymatic glycosylation of GBM

leads to leaky and thickening

also increase in GFR due to constriction of efferent arteries (can be treated with Ace inhibitors

kimmelstiel-wilson nodules

237
Q

Amyloidosis

what will stain show?

A

Cause of NephrOtic syndrome

Kidney is the most common organ of Amyloid deposition

Congo Red stain shows apple-green birefiringence

238
Q

NephrItic Syndrome

whats the hallmark finding

what causes the finding

What are the different types

A

-_Glomerular *I*nflammation and bleeding_ that leads to hematuria and RBC casts in urine

limited proteinuria (<3.5g/day)

  • deposition of immune complex triggers inflammation
  • Types: Post Strep Glomerulonephritis, Rapidly progressive glomerulonephritis (Crescentic), IgA nephropathy
239
Q

Post Strep GlomeruloNephritis (PSGN)

when does it occur and the virulence factor

Clinical presentation

-whats it look like on histo

how do you treat it?

A

Main cause of NephrItic Syndrome

  • occurs after group A, ß hemolytic strep infection of skin or throat
  • -M protein*
  • -Periorbital Edema, Cola Urine, Hypertension*
  • -*“Lumpy bumpy Hump” GRANULAR on Basement membrane
  • it usually resolves on its own
240
Q

Rapidly Progressive Glomerulonephritis (Crescentic)

what are the crescents made of?

What will the Immunoflorescence look like?

A

A cause of NephrItic syndrome that progresses to renal failure in weeks to months

Crescents in the glomerulus

-crescents consist of Fibrin and plasma proteins

Linear: Antibodies to basement membrane = Goodpasture syndrome

241
Q

IgA Nephropathy

(Berger Dz)

when do you usually get it?

A

Cause of NephrItic Syndrome

IgA immune complex deposition in Mesangium of Glomeruli

Concurrently with Respiratory or GI Tract infection (the IgA gets secreted by mucosal linings)

242
Q

Alport Syndrome

A

cause of NephrItic syndrome

inherited (X-linked) defect in Type 4 collagen

-thinning and slpitting of the GBM

isolated hematuria

Eye problems, ear problems kidney problmes,

cant see, cant pee, cant hear a bee

243
Q

Urinary Tract infection

whos at higher risk

whats in the lab findings

which bacteria cause these?

what if you have a negative culture

A

Infection of urethra, bladder (cystitis), or kidney

most commonly ascending infection, women are more risk due to shorter urethra

+ Leukocyte esterase, + nitrites,

urine culture >100k

  • E Coli > Staph saprophyticus > Klebsiella > Proteus mirabilis (pee has ammonia scent)
  • negative culture suggests Neisseria gonorrhoaeae / Chlamydia
244
Q

Pyelonephritis (acute)

how does it present?

whats in the urine

A

Infection of the kidney (usually due to ascending infection)

-fever, flank pain (Costovertebral angle)

WBC casts in urine

245
Q

Pyelonephritis (Chronic)

which abnormality usually causes this

what does this look similiar to/mimic on histo

A

when you get acute pyelonpehritis a bunch and you get atrophy and fibrosis of the tubules

-vesicoureteral reflux (relfux back into the ureters up to the kidney)

cortical scarring with blunted calyx

“thyroidization”

246
Q

Kidney stones

symptomes

what kind of stones are there and shape/associations/tx

A

Colicky pain with unilateral flank tenderness, hematuria

  • Calcium oxylate (most common): envelope,chrons dz, tx=HCTZ
  • Amonium magnesium phosphate: coffin, ureas(+) organisms: Proteus or Klebsiella tx=surgically remove (Staghorn)
  • Uric acid: rhomboid, acidic ph/hot climate/gout(duh), tx=Allopurinol
  • Cysteine: seen in children, genetic defect where you dont reabsorb Cysteine, Staghorn
247
Q

Renal Cell Carcinoma

classic symptoms

what can it be associated with

what does it look like grossly

what mutation leads to this and which chromosome is it on

A
  • hematuria, palpable mass, flank pain
  • associated with paraneoplastic syndromes (ectopic EPO, ACTH, PTHrP, renin)
  • golden yellow mass + clear cell

Loss of von hippel-lindau (VHL) suppresor gene on Chromosome 3

smoking

248
Q

Wilms Tumor

how does pt present

which mutation?

what syndrome can this be a part of?

A

Most common kidney tumor in kids

  • blastema
  • Large palpable unilateral flank mass, hematuria, HTN
  • Loss of function of WT1 or WT2

WAGR- Wilms, Aniridia(no iris), GU malformations, mental Retardation

249
Q

main cause of rhinitis

what is a major consequence it can lead to

A

adenovirus

nasal polyps

250
Q

when a child has nasal polyps what should you be thinking?

A

Cystic fibrosis

ASA (asprin) intolerant asthma

251
Q

main cause of epiglottitis

A

H. influenza

252
Q

Pneumonia

what does the sputum look like?

percusion?

3 types of pneumonia?

A

Infection of lung parenchyma

  • yellow green or rusty colored sputum
  • dull percusion
  • Lobar, Bronchopneumonia, Interstitial
253
Q

Lobar Pneumonia

which are the two most common causes

A

consolidation of an entire lobe

usually bacteria

S. Pnuemonia (95%) & Klebsiella Pneumoniae

254
Q

Bronchopneumonia

which bacteria causes this

A

scattered patchy pneumonia cetered around the bronchioles

-S. A, H. influ, S. pneumonia, klebsiella

255
Q

interstitial (atypical) pneumonia

why is it called Walking Pneumonia

What causes it

A

diffuse interstitial infiltrates

  • has very mild symptoms
  • Mycoplasma pneumonia (military recruits or college kid), Chlamydia Pnuemonia, RSV (infants) , CMV (post transplant)
256
Q

Tuberculosis

whats the PPD

primary/secondary?

A

inhalation of Mycobacterium Tuberculosis

  • caseating necrosis of lower lobe
  • Ghon complex (fibrosis and calcification)
  • PPD (+)

Secondary- reactivation of TB due to AIDs (APEX) of lung. CASEATING granulomas

257
Q

COPD

whats the spirometry readings

types

A

obstruction of getting air OUT of the lung

ForcedVC (down), FExpiratoryV1(down-down)

TLC(up) due to lung trapping of air

-Chronic Bronchitis, Emphysema, Asthma, Bronchiectasis

258
Q

Chronic Bronchitis

how does one get it

Whats the Reid index and whats the value for CB

How do they present

whats a bad thing this can lead to

A

Hyperplasia of mucus secreted glands as a result of smoking

Reid index is the thickness of mucosal gland layer to the thickness of wall btwn epithelium and cartilage. For CB its >50%

  • presents with Productive Cough, Cyanosis
  • -Cor Pulmonale (*hypoxia leads to vasoconstriction to area and shunting to other areas in lung–> failure of right heart)
259
Q

Emphysema

what imbalnace/deficiency causes this?

most common cause of this?

what are the two types? which lobes are they associated with?

whats a nickname for this?

A

Destruction of alveolar sacs

loss of elastic fibers, increased compliance, “Shopping bag’, AIrway collapse

Lack of Alpha 1 AntiTrypsin (A1AT)

-SMOKING (duh bruh)

Centriacinar (smoking-upper lobes)

Panacinar (A1AT deficiency- lower lobes)

-PINK PUFFER (barrel chest)

260
Q

Asthma

A

Reversible Bronchospasm most often due to allergic stimulus

IgE Hypersensitiviy type 1 mediated

261
Q

IL-4

IL-5

IL-10

A

4 - IG class switching

5 - calls in eosinophils

10 - stimulates th2 T cells

262
Q

Bronchiectasis

what causes it?

A

Permanant dilation of the bronchioles and bronchi

loss of tone leads to air trapping

(think of blowing throught a big pipe)

-necrotizing granulation of airway wall

secondary amyloidosis

263
Q

Restrictive respiratory DZ

whats the FEV:FVC ratio?

A

Restricted filling of the lung mostly due to FIBROSIS

Ratio is INCREASED >80%

Idiopathic pulmonary fibrosis

264
Q

Idiopathic pulmonary fibrosis

what does lung look like?

Treatment?

A

repeated wound healing with collagen deposition

Honeycomb lung appearance

lung transplant

265
Q

Pneumonconioses

A

Interstitial fibrosis due to occupational exposure

coal worker, silicosis, abestosis

266
Q

coal workers pneumoconioses

whats caplan syndrome?

Anthracosis?

A

Restricitve lung dz (fibrosis)

Black lung

macrophages laden with carbon lead to inflammation and fibrosis

caplan: rheumatoid arthritis and penumonconioses

Antrhacosis: carbon in the lung thats assymptomatic

267
Q

Silicosis

how does it affect macrophages?

whats special solely about this pneumocon.?

what part of lung does it affect? (roof and base)

A

Restrictive lung dz (pneumoconioses)

  • sandblasting, mines
  • it impairs the phagolysosome
  • its the only wone that increases chance of TB

“silica and coal are on the base, but affect the roof”

(upper lobe)

268
Q

beryliosis

A

restrictive lung dz (pneumoncon.)

exposure to beryllium in aerospace

non-caseating granulomas

269
Q

Asbestosis

where does it affect the lung

what do you look for to confirm diagnosis

A

restrictive lung dz (pneumocon)

Associated w/ shipbuilding, roofing, plumbing.

lower lobe

-asbestos (ferrunginous) bodies: golden brown rods

270
Q

Sarcoidosis

which type of lesion and where will you find them

who gets it?

what else type of cell can you see in this histo?

what values are elevated?

why does this cause hypercalcemia?

A

Restrictive lung dz

“noncasesating granuloma” in multiple organs (speccifically lung and hilar lymp nodes)

African american femal under 40yrs old

  • asteroid body
  • elevated ACE levels, CD4/8 ratio
  • due to incr. 1Alpha-hydroxylase vit D activation in macrophages
271
Q

Lung cancer

Small cell carcinoma

who gets it, where is it located, what does it produce

A

poorly differentiated small cells

Male smokers, Centrally,

may produce ACTH or antibodies against PRESYNAPTIC Ca+2 channels (lambert-eaton)

272
Q

lung cancer

Squamos cell carcinoma

Whats the big clue on histo

where is it? what symdrome?

A

Keratin pearls and Intercelluar bridging

  • Central
  • produces PTHrP (hyperCalcemia)
273
Q

lung cancer

Adenocarcinoma

who gets these/why is it special?

where is it located

A
  • characterized by glands or mucin production
  • most common cancer in Non-Smokers,

-Peripheral

274
Q

Lung cancer

Large cell carcinoma

A

-no keratin pearls, no glands or mucin

smoking,

central or periph

(grab bag)

275
Q

lung cancer

-Carcinoid tumor

what kind of cells, whats growth look like

A

well differentiated, nest of nueroendocrine cells

chromogranin (+)

polyp like growth

276
Q

Lung cancer (general facts)

where does it metastisize?

Where does it get mets from?

what complications does it cause

A

mets to the adrenals

mets from the breast, colon, prostate

SPHERE of complications

-Superior Vena Cava syndrome, Pancoast tumor, Horner syndrome, Endocrine (paraneoplastic), Recurrent laryngeal nerve (hoarseness), Effusions (plueral)

277
Q

Pneumothorax

What are the types and describe them

A

Accumulation of Air in the Pleural space

Spontaneous: Rupture of bleb or cysts. collapse of the lung w/ trachea shifting to collapse

Tension: caused by penetrating chest wall injury. trachea is pushed to opposite side of injury. (this is the one with the flap. air gets in but cant get out. pushes the trachea away)

278
Q

Mesothelioma

how does it present?

what occupational hazard can cause this

A

Malignancy of the Mesothelial cells

Presents with recurrent pleural effusions

-Asbestos

279
Q

Whats up with DiGeorge Syndrome?

whats the deletion

how does it present?

A

Developmental failure of 3rd/4th pharyngeal pouch

  • 22q11
  • -*T-cell deficiency (Lack of Thymus)
  • Hypocalcemia (Lack of parathyroid)
  • Cardiac Defects
280
Q

Whats up with SCID?

what are the deficiencies?

tx?

A

Defective cell mediated (T-cell) and Humoral mediated (B-cell) immunity

-Adenosine Deaminase Deficiency

MHC class II deficiency

-bubble boy/ bone marrow transplant

281
Q

whats up with X-linked agammaglobulinemia

whats the defect?

when do you get it? why?

A

-fuck up of B-cell maturation

complete lack of immunoglobulins

  • defect in BTK (Bruton Tyrosine Kinase)
  • After 6 months of life which is when maternal IgG depletes
282
Q

Common Variable Immunodeficiency

A

B-cell defect.

low immunoglobulin

-increased risk of autoimmune dz and lymphoma

283
Q

Selective IgA deficiency

What type of infections

A
  • low serum IgA (duh)
  • mucosal infections
284
Q

Hyper IgM Syndrome

wheres the mutation

what type of infections?

A

increased levels of IgM

mutation at CD40L (cant class switch)

-decreased IgA, IgE, IgG

Pyogenic infections, mucosal infections

285
Q

Wiskott-Aldrich Syndrome

(W.A.T.E.R)

A
  • Mutation in WAS gene
  • Wiskott Aldrich Thrombocytopenia Eczema Recurrent infections
286
Q

Systemic Lupus erythematosus

Presentation

labs?

A

Autoimmune Dz

-Malar “butterfly” Rash. Chronic inflam, Arthritis, CNS psychosis

Renal Damage (Cause of death)/ Heart problems

Libman-Sacks-Endocarditis (SLE–>LSE) Vegetations on both sides of a valve

-Antinuclear antibody (ANA) + Anti-dsDNA

287
Q

What are the Lupus causing drugs?

what antibodies do they produce?

A

Hydralazine, procainamide, Isoniazid

AntiHistone antibodies

288
Q

Anti-phospholipid syndrome

what are the two antibodies?

what can they lead to?

tx?

A

Associated with Lupus

Autoantibody associated with proteins on phospholipid. Hypercoag state

Anticardiolipin + lupus anticoagulant (falsely increases PTT)

  • false positive syphillis test*
  • -*life long anticoag tx
289
Q

Sjogren Syndrome

presentation?

lab test? what other dz is SS associated with?

what could enlarged parotids lead too?

A

Autoimmune destruction of Lacrimal and Salivary glands.

-dry eyes, dry mouth, dental carries

  • presence of ANA: Anti-SS-A/ Anti-SS-B (ribonucleoproteins)
  • Rheumatoid arthitis
  • enlarged parotids=could mean B Cell Lymphoma
290
Q

Scleroderma

Diffuse vs Localized

A

Triad: Autoimmunity, noninflam vasculopathy, Collagen depositions w/ Fibrosis

Diffuse: widespread involvement of skin and viscera. Anti SCL-70 antibody (Anti-DNA Topoisomerase I antibody)

Localized: local skin involvment of fingers and face. CREST syndrome- Calcinosis/anti Centromere ab, Raynauds, Esophageal dysmotility, Sclerodactyly, Telangeictasia

291
Q

Mixed Connective Tissue Dz

whats the antibody?

A

Grab bag of a lil bit of SLE, Scleroderma, polymyosistis

Anti-U1 RNP antibodies

292
Q

What are the layers of the epidermis? from surface to deep. what are found in each

A

Stratum Corneum (keratin)

Lucidum

Granulosm

Spinosum (desmosomes)

Basale (stem cells)

293
Q

Whats atopic dermatitis?

where does it usually appear?

what type of hypersensitivity?

A

aka Eczema

face and flexor surfaces

TYPE I

294
Q

Contact Dermatitis

what type of hypersensitivity

tx?

A

Poison Ivy, Nickel, neomycine

Type IV (delayed)

-remove offending agent/topical steroids

295
Q

Acne

whats it due to?

what type of infection

tx?

A

comedones (white heads and black heads), pustules (pimples)

Chronic inflammation of the hair follicles and sebacious glands

Proprionibacterium acnes (P. acnes)

-retinoids, benzoyl peroxide, antibiotics

296
Q

Psoriasis

whats it look like/ where is it found

whats another clinical sign it can be found with?

whats Auspitz sign?

tx?

A

excessive keratin proliferation: Parakeratosis (nuclei still in Stratum Corneum)

well-circumscribed “salmon colored” plaques with silvery scales

  • extensor surfaces and scalp
  • nail pititng

Auspitz: pinpoint bleeding after removing a scale

-corticosteroids/

297
Q

Lichen Planus

how does histo look?

which other infection is it associated with?

A

Pruritic, purple, polygonal planar papules and plaques

  • Sawtooth infiltrates of Lymphocytes at dermal-epidermal junciton
  • Hep C
298
Q

Pemphis Vulgaris

whats histo like? what layer is messed up

whats the clinical sign/finding?

what does immunoflourescence look like?

which type of skin does it involve?

A

Autoimmune destruction of Desmosomes via IgG antibodies

-tombstone appearance since basment cells are intact while the Stratum Spinosum is fucked up

  • Separation of epidermis upon touching the skin (wet blisters)
  • Net-like
  • skin and oral mucosa
299
Q

Bullous Pemphigoid

what will immunoflourescene look like?

how do the blisters look?

A

Autoimmune Destruction of Hemidesmosomes via IgG antibodies

-Linear pattern

oral mucosa isnt affected

-Tense Blisters that dont rupture easily

300
Q

Dermatitis Herpetiformis

what do the lesions look like?

what dz is associated?

how do you treat it?

A

Depositions of IgA at tips of dermal papillae.

  • -*herpes; so tiny vesicles that are grouped together
  • Celiac dz

-dapsone/gluten free diet

301
Q

Erythema Multiforme

what kind of skin lesions?

what are some associations?

A

Hypersensitivity reaction w/ Target Lesions

-HSV, M. pnuemo, sulfa drugs

302
Q

Steven Johnson Syndrome

whats TEN?

A

Erythema Multiforme w/ oral mucosa and Fever

-Toxic epidermal necrosis: Sloughing off of the skin

303
Q

Sborrheic Keratosis

whats it called when you have a sudden appearance of these?

A

morgan freeman, looks stuck on

Leser-Trelat sign: sudden onset, usually a sign of malignancy (usually GI)

304
Q

Acanthosis Nigricans

(thick epidermis) (dark)

what is it? where is it usually found?

what causes/associated with it?

A

Thickening of the skin

usually on the groin or axilla

-diabetes, obesity, cushings, malignancy

305
Q

Basal cell carcinoma of the skin

what are the risk factors?

whats it look like?

whats a key finding on histo?

tx

A

most common skin cancer

  • exposure to UV sunlight
  • raised lesion/central ulcer/dilated blood vessels (telangiectasias)
  • palisading nuclei
  • tx: excision
306
Q

Squamous cell Carcinoma of the skin

what are some risk factors?

where is it usually found?

tx

whats usually its precursos

A

malignant proliferation of squamous cells

  • sunlight, immunosupression, arsenic
  • LOWER LIP
  • excision
  • Actinic keratosis
307
Q

Actinic Keratosis

A

precursor to squamous cell

308
Q

Keratoacanthoma

A

well differentiated SCC

volcanic lesion that forms quickly and resolves quickly as well

309
Q

what level in the skin are mealoncytes found?

what embryo structure is it derived from?

where does it synthesize melain?

A

in the Basal cells

  • neural crest
  • synthesizes melanin in the melanosome
310
Q

Vitiligo

A

Autoimmune destruction of the melanocytes

  • localized loss of skin pigmentation
311
Q

Albinism

whats the enzyme defect?

what are the 2 types?

what can it lead to?

A

Congenital lack of pigmentation

–defect in Tyrosine transport (impairs melanin production)

  • eyes or eyes/skin
  • increased risk of skin cancer
312
Q

why are freckles present/darker than rest of skin?

A

they have increased number of melanosomes in their cells

313
Q

whats Melasma?

A

hyperpigmentation of the cheeks associated with pregnancy or OCP use

314
Q

Nevus (moles)

whats a junctional nevus?

A

Junctional: increased melanocytes at dermal-epidermal junction. these guys are Flat

315
Q

Melanoma

subtypes: nodular/lentiginous/acral

A

Malignant neoplasm of melanocytes

most common cause of Death in skin cancer

nodular: bad prognosis, creates huge bump
lentignious: good prognosis (radial prolif along the dermal epidermal junction)
acral: on the hands and feet of dark skinned ppl

316
Q

Impetigo

A

skin infeciton caused by SA and Strep pyogenes

Honey colored crusting

317
Q

Cellulitis

risk factors?

A

deep skin infection (bacteria to the dermis

red, tender swollen rash

-trauma, bug bite, surgery

318
Q

Necrotizing fasciitis

A

Necrosis of Subcutaneous tissue below the dermis

caused by anaerobic flesh eating bacteria

produciton of CO2 leads to crepitus

319
Q

Staph scalded skin syndrome

difference between this and TEN (toxic epidermal necrosis)

A

Exotins A&B destroy keratinoctye attachments in stratum granulosom from rest of skin

  • sloughing of skin with rash and fever
  • TEN has separation at the dermal-epidermal junction where as SSS is stratum granulosom
320
Q

which hormones do prolactin inhibit

what inhibits prolactin secretion

A

GnRH

-dopamine

321
Q

whats sheehan syndrome

what are some clinical signs

A

In pregnancy the pituitary gland doubles in size, however, the blood flow doesnt increase to match it so it doubles in size

-poor lactation and lossof pubic hair

322
Q

Condyloma

what is it? whats main cause

A

Warty neoplasm of genital area

  • HPV 6 and 11.
  • koilocytic change
323
Q

Lichen Sclerosis

A

Thinning of the epdiermis/fibrosis of the dermis of the vag

-cigarrete “parchment” paper skin

324
Q

lichen simplex chronicus

what causes it

A

hyperplasia of vulvar epithelium

  • thickening of the skin
  • chronic itching and scratching
325
Q

Pagets dz of the vulva

A

malignant epithelial cells of the epdiermis

-erythematous, pruritc, ulcerated skin

326
Q

Clear Cell Adenocarcinoma

whats an old drug that causes this?

A

Malignant proliferation of glands with clear cytoplasm

-DES

327
Q

Embryonal Rhabdomyosarcoma

A

Grape-like protrusion

malignant mesenychmal cells of immature skelatal muscle

328
Q

Lymph node spread of upper and lower vag carcinomas

A

upper 2/3 – inguinal

lower 1/3 - illiac nodes

329
Q

What causes acute endometriitis

A

left over products of conceptions

330
Q

endometrial polyps

major presentation

A

painless uterine bleeding

331
Q

Endometriosis

A

endometrial glands and stoma outside the uterine lining

332
Q

whats a chocolate cyst?

A

its when the ovary is filled by endometriosis

333
Q

Adenomyosis

A

Extension of the endometrial tissue (endometriosis) into the myometrium

334
Q

Endometrial hyperplasia

what causes it?

how does it present

most important predictor for progression to carcinoma?

A

abnormal endometrial GLAND proliferation (relative to stroma)

  • excess estrogen stimulation
  • post menopausal vaginal bleeding
  • nuclear atypia
335
Q

Endometrial Carcinoma

how does it present

A

Malignant prolif of endometrial glands

post menopause bleeding

336
Q

Leiomyoma (fibroid)

how dangerous are they?

A

Benign proliferation of smooth muscle from myometrium

multiple, well-circumscribed tumors that increase during pregnancy

-asymptomatic, but sometimes can cause bleeding

337
Q

whats the functional unit of the ovary?

A

Follicle

338
Q

Polycystic Ovariand Dz (PCOD)

what causes it?

classic presentation

what can it usually lead to?

A

hormone imbalnce -> incr. LH/ low FSH

-too much LH leads to incr. androgen production. that androgen goes to the periphery and gets converted to estrogen which then goes to pituitary and shuts down FSH (neg. feedback)

w/o FSH the ovary atrophies and creates a cyst

  • obese woman, hirsutism, infertiliity,
  • insulin resistance/diabetes
339
Q

when would you use the serum marker CA 125

A

to monitor for treatment and Recurrance

340
Q

Mature cystic teratoma of the ovaries

what type of tumor (Surface epithelia, Germ cell, Sex cord stroma)

what do the cysts contain

Immature cystic teratome

A

Germ cell

Contains fetal tissue from all 3 germ layers

Benign

______________________

Immature contains immature tissue (ie neuroectoderm)

341
Q

cystic teratoma composed of thyroid tissue

A

Stuma ovarii

342
Q

Dysgerminoma

A

malignant ovarian tumor

Sheets of uniform “fried egg” cells (large cells with central nuclei and clear cytoplasm)

343
Q

Yolk sack tumor (whats another name for it)

most common germ cell in ____

whatst the major tumor marker

what cells do you see on histo

A

Endodermal sinus tumor

most common germ cell in kids

AFP

Schiller-Duval bodies (central vessel looks like glomeruli) *glomeruloid like structures

344
Q

Choriocarcinoma

whats it composed of?

lab abnormalities?

how does it spread?

A

Malignant prolif of placenta tissue

-trophoblasts and Syncytiotrophoblasts

Villi are absent

Very high ß-hCG

-hematogenously

345
Q

Granulosa-Theca cell tumor

A

sex cord stromal tumor

neoplasm of granulosa/theca cells (duh)

production of estrogen/progestorone which will have differnt affects at different ages

346
Q

Fibroma

Associated with _____ syndrome. which is

A

Benign tumor of Fibroblsts

Meigs Syndrome: Fibroma, Ascites, Hydrothorax

347
Q

Krukenberg tumor

what does it secrete?

A

Gi malignancy that mets to ovaries

mucin secreting signet cell adenocarcinoma

348
Q

Psuedomyxoma peritonei

where does it usually come from

A

intraperitoneal accumulation of mucin material

usually arises from Appendix tumor

349
Q

Ectopic pregnancy

whats the most common site?

big risk factor?

clinical presentation

A

fertilization and implantation of ovary at site other than uterine wall.

  • ampulla of Fallopian tubes
  • scarring (from PID-salpingitis, endometriosis)
  • lower abdominal pain after missed period (ALWAYS DO PREGNANCY TEST)
350
Q

Spontaneous abortion

A

loss of fetus before 20 wks

passage of fetal tissues

351
Q

differences between

Placenta Accreta/Increta/percreta

and presentations

A

Accreta: placenta attaches to myometrium w/o penetration. difficulty delivering placenta

352
Q

HELLP syndrome

A

Preeclampsia w/ thrombotic microangiopathy of the liver

Hemolysis, Elevated Liver enzymes, Low Platelet

HELLP

353
Q

Sudden infant Death Syndrome (SIDS)

risk factors

A

Death of infant 1mo. - 1 yr. without cause

-sleeping on stomach, smoking in house,

354
Q

Hydatidiform mole

how do you diagnos

Tx?

A

instead of growing a baby you grow abnormal placental tissue

swollen and edematous villi, proliferation of trophoblasts

-passage of “grape-like” masses / snowstorm on US

-dilation and curettage of mole, monitor b-hcg

355
Q

Complete Hydatidiform Mole

whose fault? fetal parts? villi? b-hcg

A

All dads fault (only sperm and enucleated egg)

46,XX; 46, XY

  • no fetal parts
  • All villi are edematous/fucked up
  • b-hcg much higher than partial mole
356
Q

Partial Hydatiform mole

fetal tissue? villi?

A

2 sperm + 1 egg

69 XXX; 69, XXY; 69, XYY

Yes fetal parts

some villie are fucked

357
Q

What causes Hypospadias?

A

failure of the urethral folds to fuse

pee out the bottom of your weewee

358
Q

what causes Epispadias?

what other abnormality is it associate with?

A

faulty positioning of the genital tubercle

bladder Extrophy (protrusion of the bladder)

359
Q

Squamous cell carcinoma of the penis

major risk factors

precursor lesions:

A

malignant prolif of squamos cells of the penis

High risk HPV/lack of circumcision

-Bowens dz: shaft

Erythoplasia of Queyrat: glans

Bowenoid papulosis: reddish papules

360
Q

Cryptorchidism

major complication?

A

undescended testicle

-usually self resolving but after age 2 it can lead to testicular atrophy/increased risk of seminoma

361
Q

testicular Varicocele

which side is most common

A

“Bag of worms”

Dilated veins

-usually left sided due to drainage into left renal vein

362
Q

what causes testicular hydrocele?

A

incomplete obliteration of processus vaginalis (infants)

or blockage of lymph drainage (adults)

363
Q

Acute Prostatitis

buzzwords for clinical presentaiton?

Chronic Prostatis

A

-Tender and Boggy

________________

Lower back/pelvic pain

364
Q

Benign prostatic hyperplasia

what causes it

what it can lead to

tx-

A

hyperplasia of the prostate around the lateral/middle lobes. increased PSA

Not premilignant

-increase of DHT

-hydronephrosis

-tx: a-blocker (terazosin), 5a-reductase inhibitor

365
Q

Prostatic adenocarcinoma

how is it diagnosed

where does it met to?

A

Malignant prolif of prostatic glands

Most common cancer in men

arises in peripheral zone

-diagnosed by Incr. PSA / decr. fraction of free PSA

-mets to the bone (lower back pain)

366
Q

What are the lobules and ducts lined by in the breast?

A

luminal cell layer

myoepithelial cell layer (contractile function)

367
Q

Acute Mastitis

which organism causes this

A

Staph Aureus.

infection of the duct, purulent discharge

368
Q

Fat necrosis

what does the biopsy show?

A

benign lump due to injury to breast tissue

necrotic fat with calcifications and giant cells

369
Q

Fibrocystic changes

A

most common in premenopausal women

lumpy breasts, Blue dome cysts

370
Q

whats Sclerosing adenosis

A

fibrosis of the acini and stroma of the breast

associated with calcifications

371
Q

Intraductal papilloma

most common cause of _________

A

papillary= long like finger pertrusion in the lactiferous duct

most common cause of BLOODY NIPPLE

372
Q

Fibroadenoma

estrogen sensitive?

A

Most common tumor in premenopausal females

tumor of fibrous tissue and glands

well circumscribed, mobile, marble like

-yes

373
Q

Phyllodes Tumor

A

benign breast tumor with Leaf like lobulations

374
Q

Ductal carcinoma in Situ (breast)

how is it detected on mammography

whats the comedo subtype

A

Malignant proliferation of cells in ducts

  • No invasion* into the basement membrane
  • micro calcifications

-Comedo:high grade cells w/ necrosis and dystrophic calcification in center

375
Q

Paget’s dz of the breast/nipple

how does it present?

A

DCIS that extends to the nipple

-nipple ulceration/erythema

376
Q

Invasive ductal Carcinoma (breast)’

advanced tumors can cause ____

A

forms rock-hard“duct like” structures

-dimpling of skin / retraction of nipple

377
Q

Inflammatory breast cancer

what does the breast look like?

prognosis

A

Cancer of the Dermal lymphatics

Peau d’orange (breast dimples like orange skin)

Large boob

pretty bad prognosis

378
Q

Invasive lobular carcinoma

how does it look?

A

Orderly row (Indian file) of cells due to decr. E-cadherin

379
Q

Whats a pleomorphic adenoma

whats it composed of?

where does it usually arise?

whats the tumor look like? special about it?

A

A bening mixed tumor of the salivary glands

  • most common salivary gland tumor
  • composed of stromal and epithelial cells
  • parotids
  • mobile, painless, and circumscribed
  • high rate of recurrance
380
Q

Warthin Tumor

A

benign cystic tumor with germinal centers

-contains lymphnode tissue

381
Q

Mucoepidermoid carcinoma

A

most common malignant tumor of the salivary glands

-mucinous and squamous components

Brain Gainz (30 decks)

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