Professional Documents
Culture Documents
Goljan Audio Transcript
Goljan Audio Transcript
GoljanPathologyReview
MostpopularresourseforUSMLEStep1
ComprehensivePathologyReview
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
TPR = V/r
37
38
pH = [HCO3-] / pCO2
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
MC mets to adrenal = lung therefore they always do a CT of the hilar lymph nodes, and
adrenal glands in the staging of all lung cancers.
Bone = blastic, therefore the most likely cause is prostate cancer.
VIII. Stains and EM used to help dx dz:
Stains: desmin good stain for muscle ie used for rhabdomyosarcoma
Stain for keratin (most carcinomas have keratin in it, therefore stain for that)
Stains help ID diff types of tumors
Vimentin- mesenchymal cells
EM: Used when nothing else helps
Auput tumor see neurosecretory granules.
Histiocyte tumor (ie histiocytosis X) see birbeck granules, with CD 1
Muscle see actin and myosin filaments
Vascular malignancy Wibble palad bodies (have vWF in them); they are of endothelial origin
59
60
61
62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
Iron
LOW
LOW
NL
HIGH
TIBC
HIGH
LOW
HIGH
LOW
% saturation
LOW
LOW
HIGH
HIGH
Ferritin
LOW
HIGH
HIGH
HIGH
78
79
80
81
82
83
84
85
86
87
88
89
90
91
92
93
94
95
96
97
98
99
100
101
102
103
104
105
106
107
Platelet Count
NL
LOW
LOW
NL
NL
NL
LOW
Bleeding Time
HIGH
HIGH
HIGH
NL
HIGH
NL
HIGH
PT
NL
NL
NL
NL
NL
HIGH (W)
HIGH
PTT
NL
NL
NL
HIGH
HIGH
HIGH (H)
HIGH
108
109
110
111
112
1. Hyaline arteriosclerosis is a small vessel dz; lumen is narrow; whenever there is a lot of pink
staining stuff, this is hyaline. Example: small vessel dz of diabetes and HTN two major dzs that
produces a small vessel dz with different mechanisms:
a. Diabetes: nonenzymatic glycoslyzation aka HbA1c; glycoslyzation is glucose attaching to aa
and protein. For HbA, its glucose attaching to aa and HbA, and the HbA is glycosylated. HbA1c
levels correlate with the blood glucose levels of the last 6-8 weeks, so this is the best way of looking
at long term glucose levels. All the damage seen in diabetes is due to glucose. For a diabetic, you
should be under 6%, meaning that you are in a normal glucose range. There is nothing unique
about diabetes except for a large glucose level, you keep that normal, and its as if you dont have
diabetes. The only two pathologic processes are this: nonenzymatic glycosylation of small
BVs including capillaries in the kidney, and osmotic damage. Those tissues that contain aldose
reductase lens, pericytes in the retina, schwann cells all have aldose reductase and can convert
glucose into sorbitol and sorbitol is osmotically active sucks water into it and those cells die, leading
113
114
115
116
117
118
119
Audio Cardiovascular 2
CHAPTER 7: CARDIOVASCULAR
THE HEART
I. Hypertrophy of the Heart:
120
121
122
123
124
125
126
127
128
129
130
131
132
133
134
135
136
137
CHAPTER 8: RESPIRATORY
I. A-a gradient know how to calculate:
Alveolar O2 and arterial pO2 are never the same. The difference between the two is called
alveolar arterial gradient. Reasons for it: (1) Ventilation and perfusion are not evenly matched
in the lungs. When standing up the ventilation is better than perfusion in the apex, whereas
perfusion is better than ventilation at lower lobes. This explains why almost all pulmonary
infarctions are in the lower lobes perfusion is greater there. Also, this explains why
reactivation TB is in the apex TB is a strict aerobe and needs as more O2, and there is more
ventilation in the upper lobes (higher O2 content). Normally, alveolar O2 is 100 and the arterial
pO2 is 95. So, normally, the gradient is 5 mmHg. As you get older, the gradient expands, but
not that much. Most people use their upper limit of normal in other words, have a very very
high specificity of 30 mmHg. If you have an A-a gradient of 30 mmHg or higher there is a
problem. It is very high specificity (aka PPV truly have something wrong). The concept is
easy you would expect the gradient btwn the alveolar O2 and the arterial O2 to be greater if
you have primary lung dz. What will do this? Ventilation defects (produces hypoxemia, and
therefore prolongs the gradient dropping the PO2 and subtracting, and therefore a greater
difference btwn the two), perfusion defect (ie pul embolus), and diffusion defect. But the
depression of the medullary resp center by barbiturates does not cause a difference in A-a
gradient. So, prolonged A-a gradient tells you the hypoxemia is due to a problem in
the lungs (vent perfusion/diffusion defect). A normal A-a gradient tells you that
something outside the lungs that is causing hypoxemia (resp acidosis in resp
acidosis, PO2 will go down). Causes of resp acidosis: pulmonary probs (COPD), depression
of resp center (obstruct upper airway from epiglottitis, larygiotracheobronchitis, caf coronary
(paralyzed muscles of resp), Guillain Barre syndrome, amyotrophic lateral sclerosis, and paralysis
of diaphragm. These all produce resp acidosis and hypoxemia, but the A-a gradient will be
NORMAL). So, prolonged A-a gradient, something is wrong with the lungs. If A-a gradient is
normal, there is something OUTSIDE of the lungs that is causing a resp problem.
Few things must always be calculated: anion gap (with electrolytes) and A-a gradient for blood
gases all you need to do is calc alveolar O2. We can calculate the A-a gradient = 0.21 x
713 = 150 (0.21 is the atmospheric O2; and 760 minus the water vapor=713). So, 150 minus
the pCO2 (given in the blood gas) divided by 0.8 (resp quotient). So, normal pCO2 = 40,
and 40/.8=50 and 150-50 = 100; so, now that I have calc the alveolar O2, just subtract the
measured arterial pO2 and you have the A-a gradient. This is very simple and gives a lot of info
when working up hypoxemia.
II. Upper Respiratory Disease:
A. Nasal Polyps:
3 diff types of nasal polyps MC is an allergic polyp. Never think of a polyp in the nose of
kid that is allergic as an allergic polyp. Allergic polyps develop in adults after a long term
allergies such as allergic rhinitis Example: 5 y/o child with nasal polyp and resp defects,
138
139
140
141
142
143
144
145
146
147
148
149
150
151
152
153
154
155
156
157
158
159
160
161
162
163
164
165
166
167
168
169
170
171
172
173
174
175
176
177
178
GALLBLADDER DZ
I. Ask about pathogenesis of stone too much cholesterol in bile or too little bile salts.
You will have a supersaturated stone with cholesterol will get cholesterol stone (MC stone).
179
180
181
182
183
184
185
186
187
188
189
190
191
192
193
194
195
196
197
198
199
Amenorrhoea
200
201
202
203
204
205
206
207
208
209
210
211
212
213
214
215
216
217
218
Gestational Diabetes
Def: Woman who did not have diabetes, but after becoming pregnant develops diabetes.
Risk factors for baby:
RDS, premature delivery
Women with GD, are at a higher risk for developing diabetes later on.
Amyloid in Beta islets: Type 2
Antibodies against islets; inflammation: Type1
(Coxackie virus implicated)
HLA correlation: HLA DR3 and DR4=Type 1; propensity for developing Type 1, if certain
environmental factor comes in such as infection: Coxsackie, mumps, EBV
HLAB27: Ankylosing Spondylitis
Env factors:
Chlamydeal Infection
Ulcerative Colitis,
Shigellosis
Psoriasis
Musculoskeletal System
Need to identify crystals in synovial fluid
Gout
Pseudogout
Rhomboid crystals in synovial fluid==pseudogout
But Pseudogout could also have needle-shaped crystals (like those of mono-sodium urate in Gout)
which makes DD difficult. So you use a special filter to make the whole slide red and then the crystals
are made to look yellow or blue.
When the color of the crystals is yellow when the plane of filter is parallel to the analyzer= Negatively
birefringent =GOUT
East west direction: color is blue and parallel to analyzer=Positively birefringent = PSEUDOGOUT
(calcium pyrophosphate)
Arthritis
Osteoarthritis
Progressive wearing down of articular cartilage
219
Sometimes leads to reaction to injury: SPUR formationat the margin of the joint= Heberdens node:
osteophyte in the joint
Note the enlargement of the DIP (Heberden's nodes) and PIP joints (Bouchard's nodes), enlargements
represent osteophytes.
Rheumatoid Arthritis
Inflammatory joint dz; enlarged MCP joints
Rh factor sets up the inflammation: IgM Ab against IgG. IgG is in synovial fluid. IgM-IgG form
complexes, activate the complement system, damage the joint, synovial fluid gets inflamed, starts
growing and growing, starts growing over the articular cartilage= PANNUS; hyperplastic synovial fluid.
(different from Tophus)
Joints can get fixed, and ankylosed and cannot move.
Dont get fixing of the joint in OA.
If rheumatoids dont keep moving their joints, and if it is not controlled using anti-inflammatory drugs
then eventually they cannot move it at all.
Slide: Rheumatoid nodules. Can be seen in Rheumatic fever as well.
Example: older pt having trouble eating and swallowing crackers, feels like there is sand in my eye all
the time. On examination: eyes and mouth are dry. Dx? Sjograns Syndrome. Pt with RA and autoimmune destruction of lacrimal glands, salivary glands. Keratoconjunctivitis sicca
Rheumatoid nodules in lung + pneumoconiosis==Caplan Syndrome
Treatment of RA= Methotrexate
Example: Pt with RA, develops a macrocytic anemia with hypersegmented neutrophils, neuro exam is
normal, interstitial fibrosis in lung. What is the drug? Methotrexate
Gout = podagra
Big toe, usually first one to be involved; usually at night.
Monosodium urate crystals are precipitated and taken up by the neutrophils that phagocytose it and
release chemicalsinflammatory reaction.
Dont define Gout based on Uric acid level. Elevated uric acid does not necessarily lead to gout. About
25% of people might have elevated uric acid.
Dx: HAS to be by presence of uric acid crystals in the joint.
Treatment: Indomethacin to control inflammation.
Cause: over production (Rx=allopurinol: blocks Xanthine oxidase) or under excretion of uric acid
(>90% of cases) Rx=uricosuric drugs like probenecid and Sulfinpyrazone
220
221
Bone Disorders
Osteogenesis imperfecta
Slide: Kid with an eyeball, blue sclera: AD disorder with defect in synthesis of type I collagen, note the
blue sclera- loss of collagen in sclera allows bluish color of choroidal vessels to shine through:
Osteogenesis imperfecta (NOT foreign body!) brittle bone disease cant break bone down
Question: whats the defect? Defective synthesis of type 1 collagen
Question: whats the mechanism of development of blue sclera?
Collagen in sclera, type 1 is defective, so it is so thin, so you can see the underlying choroidal veins
that gives the blue color.
222
223
Osteogenic sarcoma
Slide: Note metaphyseal origin of the cancer and extension into the muscle, note the splinter of
periosteum that is elevated which would correspond to Codman's triangle
Slide: X-ray of proximal humerus showing the "sunburst" appearance of osteogenic sarcoma that is
extending into the muscle, osteogenic implies that the cancer is making bone
Adolescent, sun burst app, codmans triangle, knee area==Osteogenic Sarcome
Suppressor Gene relationship: Rb suppressor Chromosome 13
Muscular Disorders
Duchennes Muscular Dystrophy
Gowers maneuver
Elevated Serum CK, Absence of dystrophin protein
Sex linked recessive, missing Dystrophin gene
Variant: Beckers dystrophy: make dystrophin but it is defective
Analogy: alfa 1 antitrypsin def: MCC of HCC in children
Adults get panacinar emphysema: many diff sub types of alfa 1 anti-trypsin:
1) Absent alfa 1 anti-trypsin: get pan acinar emphysema.
2) Alfa 1 anti-trypsin is present but it cannot get OUT of the hepatocytes: so get HCC
Audio file Day 5 #5 Skin
Myotonic dystrophy - MC adult dystrophy, AD
Triplet repeat dz repetition of tri-nts (there are 4 dzs with this abnormality HD, Fragile X have
macrorchidism (big testes in adolescents), Friedrichs ataxia, Myotonic dystrophy).
In future generations, dz gets worse anticipation. Therefore, can anticipate that in future dzs it will
get worse. For each generation, there are more triplet repeats added on, leading to a more defective
protein and the dz gets worse and worse.
Example: genetic counselor telling couple that they have a dz, where if are to have children, the dz will
be fatal in their children. The couple didnt listen to their counseler, had a child and the child died only
after 1 month. What was it and what is this: an ie triplet repeat disorder (anticipation) Muscle
weakness in face (so mouth is drooped open).
Example: pt with failure to release grip on golf stick (or when shaking hand) they cannot relax their
muscle grip, diabetes, cardiac abnormality
224
225
Skin
Basal cell carcinoma (upper lip)
Squamous cell carcinoma (lower lip)
Psoriasis silvery lesion that is red and raised. Can involve the hands, scalp pts think they have
dandruff (aka seborreic dermatitis from malasezia furfura), but they really have psoriasis. On black
person wont see red lesion, will see silver one. Rash at pressure points esp the elbow.
Atopic dermatitis child with allergic diathesis starts dz; have eczema (aka atopic dermatitis); type I
HPY.
Contact dermatitis ie to metal (nickel); type IV HPY
Example: pathophys is equalant to what? + PPD, bc both are type IV HPY
Seborrheic Dermatitis
Due to Malassezia furfur (a fungus)
IC pt (ie AIDs)
This is a preAIDs lesion
Tinea capitis
Example: pt with bald spot on head, fluouresces and seen with black light blacklight (UV-A light)
Can cause Tinea capitis (now Trichophyton tonsurans is MCC)
Bc the fungus involves the inner portion of the shaft, there are no fluorescent metabolites, and is
Wood light negative
All the other superficial dermatophyte infections including Tinea corporis (ring worm)
Example: red outer edge and clear center, what is first step in workup? Scrape outside and do KOH
prep, and see hyphae and yeast forms. All other superficial dermatophyte infections (except
Tinea capitis) are due to trychophyton rubra. What is the color around Tinea capitis? Red (=
rubra) (how to remember it).
Molluscum contagiosum
Sandy like material in crater, children, self inoculate
Poxvirus makes these (DNA virus)
Volcano crater look, with sandy stuff in it
Pityriasis Rosea
226
227
228
229
Papilledema
Any cause of increased incranial pressure
Vit A tox
Lead poisoning delta-aminolevulinic acid leads to increased permeability
Audio file Day5 #6 CNS
Hydrocephalus
MCC = stenosis of the aqueduct of sylvius
Noncommunicating.
Get hydrocephalus bc the sutures have not fused
if you miss hydrocephalus in adult and sutures have fused, will lead to dilatation of the ventricles and
eventually over years, the pressure will turn back to normal bc the increased pressures keep the
choroid plexus from making so much
Dementia, ataxia, urinary incontinence.
Aka normal pressure hydrocephalus (bc pressures normalize)
Tuberous Sclerosis
AD
Hamartomas (noneoplastic proliferation of things)
Ventricles have bumps called tubercles which are hamartomas which have proliferation of astrocytes.
They produce hamartomas that bulge into the ventricle, called candle stick dripping. Hemartomas of
the kidney called angiomyolipomas, MR, cardiac tumors (rhabdomyomas), shagreen patches, areas of
hypopigmentation, woods light shine out
Anencephaly
Worst of neural tube defects
Absent brain
Vertebral arch defects
Spina bifida occulta tufts of hair come out, vert arches do not touch, no meninges come
Meningoceole meninges come out
Meningomylocele both meninges and spinal cord come out
High alpha feto protein levels in blood of mother; decreased in downs syndrome
Have to be on folate to prevent neural tube defects (neural tube finished forming by 30 days, so make
sure she is on folate if she is trying to get pregnant).
Neurofibromatosis
Albright syndrome (precocious puberty, caf au lait, bone zits)
Sturge weber
Caf au lait (coffee colored non raised lesions) spot, plexiform neurofibromas, hyperpigmentation in
the axilla (axillary freckling), neurofibromas
AD , therefore late manifestations (esp for neurofibromatosis), penetrance, variable expressivity (you
are expressing the dz, but diff levels of how severe the dz is)
Example: pt with HTN and pic, what test would you get? Relationship of neurofibroma with
pheochromocytoma, therefore get a 24 hr urine for VMA and metanephrine.
230
Acoustic schwannoma
Example: pt with sensorinerual hearining loss b9 tumor of Schwann cells around CN 8
Meningiomas
Optic nerve gliomas
Syringomyelia
Example: pt that works in factory and one of workers says you are burning your hand and pt didnt
notice this, on exam loss of musculature (loss of LMN) in intrinsic muscles of the hand, loss of pain and
temp in cape like distribution across back.
Cant feel pain (not ALS in ALS, first place of development of loss of muscles is here, so dont
confuse; but ALS is UMN and LMN loss, PURE MOTOR , so if pt has pain, ie, this is sensory and not
ALS)
Big cystic cavity knocking off spinothalamic knocking off pain and temp. can knock off the
corticospinal tract and anterior horn cells, so it will be a COMBO of sensory AND motor loss for
syringiomyelia.
Infections
Meningitis vs encephalitis
Meningitis inflammation of meninges and nuchal rigidity; if you move your head or extend your knee,
you will stretch the meniges, leading to pain (stretching inflamed meninges).
Encephalitis sleeping sickness they are always sleeping and drowsy; they have mental status
abnormalities (not nuchal rigidity)
Pus at the base of the brain can possibly block lushka and majendie, leading to obstructive
hydrocephaly and noncommunicating
When you Rx meningitis, use steroids and Abs. why? Steroids prevent scar tissue formation and
complications that arise with it (ie hydrocephalus).
This is standard TB meningitis Rx (TB in brain causes vasculitis and scarring)
Deafness is a complication of meningitis.
Rabies
Example:: meningitis, cerebral abcess, Rabies (MCC in States = skunks, dogs in 3rd world)
Negri bodies (perkinje cell inclusion)
CMV
Periventricular calicifications
Example: section of kid (brain) - see white stuff going around ventricles
MC congental infection = CMV
What body fluid is best to culture from? Urine
Meningitis
What is MC meningitis/sepis in first month of life? Group B strep strep agalactae bc many women
have this organism in their vagina, so they are carriers. Premature ruptured membranes lets the
organism get up, get an chorioamnionitis and into the bloodstream.
231
232
Hydrocephalus Ex Vacuo
Severe atrophy of brain and ventricles look bigger than they should be
Dementia
Alzheimers Dz
233
234