Hyperparathyroidism MEN2A and 2B Syndromes Stages of Pneumonia

 MEN is characterized by a
 Consolidation
predilection for rumors involving
 1st 24H
two or more endocrine glands
 Cellular exidates containing

neutrophils, lymphocytes and
fibrin
 Caoillaries are congested
 Infections spread to the hilum
and pleura – pleurisy

 Red Hepatization
 2-3 days
 Consistency of the lungs
resembles liver
 Lung becomes hypeamic
 Alveolar capillaries – engorged
with blood
 Fibrinous exudates fill alveoli
 Prsence of many erythrocytes,
neutrophils and epithelial and
fibrin
 Grey Hepatization
 2-3 days after RH
 Avscular stage
 Lung appears gray-brown to
yellow – fibrinopurulent
exudates, disintegration of red
cells and hemosiderin
 Resolution
 Resorption and restoration of the
pulmonary architecture
 Large number of macrophages
 enter the alveolar spaces
Valvular Heart Diseases Infective Endocarditis
Mitral  RHD -leading cause  Prototypic lesion- vegetation (mass of of
Stenosis  S/Sx: Dyspnea, fatigue and decreased exercise tolerance platelets, fibrin, MO’s, and scant
 PE: Irregular pulse casued by AF and signs of left and right sided HF inflammatory cells
 Malar flush with blue facies
 Oral cavity, skin and upper respiratory
Mitral  Acute MR: due to ACS w/ papillary muscle rupture, chest trauma, tract are the primary portals
regurgitation endocarditis  HACEK
 Chronic MR: due to RHD, MVP, cardiomyopathies 1. Haemophilus sp
 Murmur: Apical holosystolic murmur of at least grade III 2. Aggregatibacter
Mitral valve  Frquent finsing in inheritable connective tissue d/o 3. Cardiobacterium hominis
prolapse  Floppy valve syndrome/ Barlow’s syndrome 4. Eikenella corrodens
 Murmur: apical mid or late non-ejection systolic murmur preceded 5. Kingella kingae
by a click
Aortic  Most comm cause is degenerative calcification of aortic cusps  Janeway lesions – classic
stenosis  Cardinal symptoms: nonsuppuartive peripheral
1. Exertional dyspnea manifestations of subacute endocarditis
2. Angina
3. Syncope
 Pulsus parvus et tardus- weak and late peaking delayed pulse
 Murmur: Ehection mid systilic crescendo-decrescendo murmur
shortly after S1ults

Aortic  Can be caused by primary aortic valve diseaseor primary aortic root
regurgitation disease
 Acute AR: (endocarditis, aortic disss): Pulmonary edema and
cardiogenic shock
 Chronic AR: long asymptomatic period while LV gradually enlarges,
then symptoms develop- palpiatations, exert. Dyspnea, HF
 Austin Flint murmur - soft low-pitched rumbling mid to late diastolic
murmur at apex
 De Musset sign – jarring of the body and bobbing of the head with
 each systole in severe AR
 Quincke’s pulse - visible capillary pulsations at the root of the nail
with pressure
 Traube sign – booming pistol shot sound over femoral arteries
 Duroziez sign – to and for murmur when femoral artery is
compressed
 Muller sign – systolic pulsations of the uvula
 Water- Hammer(Corrigans pulse) – bounding and forceful pulse,
rapidly increasing and collapsing

Triscupid  Gen. rheumatic in origin

stenosis  Graduaaly developing

Nephrotic syndrome Pheochromocytoma Child Pugh score

 Well vascularized tumors that arise  Used to assess prognosis of chronic liver
form cells derived from the
disease- cirrhosis
sympathetic (adrenal medull or
sympathetic trunk) or  Includes:
parasympathetic (carotid body , 1. Serum bilirubin
glomus tymapnicum, glomus 2. Serum albumin
jugulare, glomus vagale) paraganglia 3. Prothrombin time
 Paraganglioma – catecholamine 4. Ascites
producing tumors in the skull base 5. Hepatic encephalopathy
and neck  Class A- 5-6 score
 The ‘’ great masquerader’’  Class B 7-9 score
 TRIAD: Palpitation, headache and  Class C 10-15 score
profuse sweating  >7 score – accepted score for liver
 Dominant sign is HTN
 Dx: Catecholamine excess and transplant
localization of tumor by imaging
 Elevated plasma and urinary levels
 of catecholamines and
metanephrines form the
cornerstone of dx
 Histo: Zellbalen pattern – nests of
neuroendocrine chief cells with
peripheral glial-like sustentacular
cells
Meckel’s Diverticulum

Diagnosis of Acute Hepatitis

Diagnostoc HBsAg IgM Anti HAV IgM Anti HBc Anti HVC
interpretation
Acute + - + -
Hepatitis B
Acute hepatitis + + - -
A and B
Acute hepatitis + + + -
A and B
Acute hepatitis - + - -
A

Acute - - - +
Hepatitis C

Hepatitis Explanation

GCS Beck’s triad Cardiac Tamponade

Acute Pancreatitis
ADPKD
 PKD Genetically heteregenous
disorder
 Leading cause of kidney failure
 Progressive formation of epithelial
lined cyst
S/Sx:
 Progressive bilateral renal cyst
 HTN
 abdominal masses
 Back or flank pain- frequent symptom,
Gross hematuria (40%) of patients
Dx:  HHS
 Presence of at least 2 renal cyst (uni or
bilat) is suff (15-29)
 Presence of at least 2 cyst in each
kidney and at least 4 cysts in each
kidney are required (30-59 and 60 or
older)
Tuberous Sclerosis
 Rare autosomal dominant syndrome
caused by mutation of 2 genes TSC1-
hamartin TSC2- tuberin
 Kidney cysts- frequent
 2 other conditons: Kidney growth,
Renal cell carcinom, Renal
angiomyolipomas- most common
kidney finding in TS - multiple and
bilateral
ARPKD
 Disease in children
 Diagnosed in utero
Von Hippel Lindau Dis
 Inherited cancer syndrome with renal
manifestations
 Autosomal dominant
 Mutation in VHL tumor suppressor gene
 Multiple bilateral kidney cysts
 Nonrenal: Pheochromo, Cerebellar
hemangioblastoma, retinal hemangioma
DKA
 Nausea and vomiting- prominent
Kussmaul resp
 Fruity odor on pts breath - sec to
metabolic acidosis and increased acetone
 Cerebral edema- serious compl most
seen in children
 DKA - hyperglycemia, ketosis, metab
acidosis (incr anion gap)
 Elderly w/ T2DM sev week hx of polyuria,
weight loss, and diminished oral intake
 Mental conf, lethargy or coma
VTE Functional classification RA
 
Virchows triad  ClassI: Pts with cardiac disease but w/o  Chronic, inflammatory dis, marked by
 Inflammation resulting limitations to physical activity symmetric, peripheral polyarthritis
 Hyper coagulability  Class II: cardiac dis= slight limitation;  Early morning joint stiffness lasting more
 Endothelial injury comfortable at rest, ordinary physical than 1 hr that eases w/ physical activity
Naturally occurring coagulation inhibitors: activity results in fatigu etc  Joint involvement: initially monoarticular,
 Antithrombin  Class III: cardiac dis=marked limitation; oligoarticular (<4 joints), polyarticular
 Protein C comf at rest; less than ordinary causes (>5joints), symmetric distribution
 Protein S fatigue etc  Most freq inv joints: wrist, MCP, PIP
Blood tests:  Class IV: cardiac dis =inabilty to carry  Flexor tendon tenosynovitis - freq
 Plasma D-dimer ELISA any physc ativ hallmark - trigger fingers
 More specific with PE  Swan neck deformity
ECG  Boutonneire deformit
 S1Q3T3 sign  Z line deformity
 S wave in lead 1, Q wave in lead 2,  Piano key movement
inverted T wave in lead 3  Flat feet
CXR  Pleuritis- most commpulm manifestations
 Westermark’s sign - focal oligemia of RA
 Hampton’s hump - wedged shaped  Pericardium - most frequent site or
density above the diaphragm cardiac involvement
 Palla’s sign- enlarged right descending  Felty’s syndrome - triad of neutropenia,
pulmonary art splenomegaly, nodular RA
 Most comm cause of death w/ RA -
cardiovascular dis

Epidural Hematoma Subdural hematoma Subarachnoid

 Arterial hemorrhage between the dura  Venous hemorrhage  Rupture of berry aneurysm I the circle of
and skull  Laceration of bridging veins willis
 Res from skull fracture and laceration of  Gradual signs of cerebral compression
middle meningeal artery  
  Lucid interval fol by loss of
consciousnessand signs of cerebral
compression

Polymyalgia rheumatica Fibromyalgia Killip scoring for prognostication

 Closely assoc w/ giant cell arteritis  Chronic, widespread musculoskeletal Class I  Normal BP 0-5%
 Stiffness, aching and pain in the muscles pain and tenderness  No rales or signs of
of the neck shoulder, lower back hips and S/Sx pulm congestion
thigh  Pain all over Class II  Mod HF 10-20%
   Poorly localized  + bibasal crackles
 Difficult to ignore  Normal BP
 Dx: pain must be present most of the  S3 gallop
the day on most days for at least 3  Tachypnea or signs of
mos right sided HF
 
Class III  Severe HF 35-45%
 Mid basal rales and
pulm edema
 S3 and S4
 Normal BP
Class IV  Shock with BP <90 85-95%
 Peripheral cyanosis
 Mental confusion
and oliguria
Scleroderma (Systemic sclerosis) COPD
 Uncommon connective tissue d/o chara  Airflow limitation that is not fully
by multisytem involvement, reversible
heterogenous clinical manifestations  Centriacinar emph - assoc w/
 Thickened skin - distinguishing hallmark
 CREST syndrome - Calcinosis cutis,
Raynaud’s phen, Esoph dysm,
Sclerodactyly, Telaginectasia
cigarette smoking; prominent in
upper lobes
 Panacinar emph - pts with a1
antitrypsin def with predilection to
lower lobes
 Airflow limitation- major physiologic
change in COPD
 Elastin critical in the integrity of the
of the lung
 Major site of inc resistance in pts
with COPD <2mm in diameter
 Reduced FEV1to FVC ratio
 Cigarette smoking - major risk factor
for mortality from CB and E
 Smoking cessation, O2 therapy and
lung reduction- influence natural hx
of pts with COPD
 Supplemental O2 is the only
pharmacologic therapy
demonstrated to dec mort

Emphysema Chronic Small

bronchitis airway
disease
 Destruction  Chronic  Small
and cough bronchiol
enlargement and es are
of lung phlegm narrowed
alveoli
 Destruction
of gas-
exchanging
air spaces
1. Respi
 bronchiole
s
2. Alveolar
ducts
3. Alveoli

Framingham Criteria Pneumonia DM meds