papilledema

causes of papilledema

edema and hyperemic of the optic disc

1. raised ICP
2. malignant hypertension
3. cavernous sinus thrombosis

Grade I papilledema is characterized by a C-shaped halo with a temporal gap

With Grade II papilledema, the halo becomes circumferential

Grade III papilledema is characterized by loss of major vessels AS THEY LEAVE the disc (arrow)

Grade IV papilledema is characterized by loss of major vessels ON THE DISC.

Grade V papilledema has the criteria of grade IV plus partial or total obscuration of all vessels of the disc.

reference: dorland dic, OHCS, eye rounds.org

abdominal pain

presenter: isya
dr Mular

52 yr old chinese gentleman was admitted on 11/7/11 at 4B

problem lists:
1)abdominal pain 3/52
3 weeks duration of progressingly worsening and fluctuating squeezing pain at the upper abdomen.
the pain disturbing patient sleep with no aggravating and relieving factor.
3 days PTA, loose stools and tenesmus
associted with LOA & LOW and progressively become lethargy.
no nausea, no vomiting, no PR bleed, no jaundice, no pale colored stool

2)low grade fever 3/52
intermittent
fever at evening and night,relieved by PCM

no hx of blood transfusion, no tatto

history of multiple sexual partners, and sexual partner with multiple sexual partner

had color vision deficit, red-green, otherwise no DM, no HPT no Asthma.

past surgical/drug/allergy-nil

past family hx: both parents die due to cx of DM and HPT.no fhx of malignancy

social hx: married with 3 children, A&W
smoke for 60 pack-year
consume alcohol for 20 yrs(2 bottle of beerx2/week)
working as mechanic with income of 2k-3k

0/E
pt well, pink orientated to TPP, no in respiratory difficulty, not complaining any pain

vital signs normal

abdominal examination:
distended epigastric and periumbilical
soft abdomen, tenderness over the epigastric, RHC,r.lumbar and RIF.
firm liver mass,6cm from costal margin, smooth surface with prominent hard nodule at the epigastric region, tender, no bruit
liver span:16cm

spleen, kidney, not palpable.

no ascites

normal bowel sound

refused for DRE

CVS, respi-normal

Differential dx:

1: 2ndary mets to the liver from gi
more common than primary
hx of loa,low
liver mass

2. primary liver ca
loa, low
liver mets
risk for hepatitis

3.pyogenic liver abscess
tender liver mass.

4.hemangioma of the liver

5. benign liver tumor

6. liver cyst

ix:

blood ix:
1. fbc tro inflammation/infection
2. LFT
3. CEA
4. AFP

imaging
1.abdominal u/s
2. CT scan

diagnosis
1. liver mets fr GI malignancy
2. diverticulis

hemolytic anemia: schistocytes; spherocytosis; bite cells; blister cells

Hemolysis may be either intravascular or extravascular.

In intravascular hemolysis RBCs lyse in the circulation releasing hemoglobin into the plasma. Causes include mechanical trauma, complement fixation, and other toxic damage to the RBC. The fragmented RBCs are called schistocytes.



In extravascular hemolysis RBCs are phagocytized by macrophages in the spleen and liver. Causes include RBC membrane abnormalities such as bound immunoglobulin, or physical abnormalities restricting RBC deformability that prevent egress from the spleen. Extravascular hemolysis is characterized by spherocytes.Spherocytes are small, spherical red blood cells (RBC). Spherocytes are approximately two-thirds the diameter of normal RBC.¹ In comparison to normal erythrocytes, they have a decreased surface area to volume ratio. They are more densely hemoglobinized and lack a zone of central pallor.

Intravascular hemolysis releases hemoglobin which is immediately bound by haptoglobin.

Hemoglobin-haptoglobin is cleared almost immediately from the plasma by hepatic reticuloendothelial cells.

As intravascular hemolysis with binding to haptoglobin generally overwhelms the rate of haptoglobin synthesis, haptoglobin levels decrease.

After haptoglobin is saturated, excess hemoglobin is filtered in the kidney and reabsorbed in the proximal tubules where the iron is recovered and converted into ferritin or hemosiderin.

Hemoglobinuria indicates severe intravascular hemolysis overwhelming the absorptive capacity of the renal tubular cells.

Urine hemosiderin is another indicator that intravascular free hemoglobin is being filtered by the kidneys.

Lactic dehydrogenase (LDH) is greatly elevated in patients with intravascular hemolysis.

Note: Haptoglobin, synthesized by the liver, is decreased in patients with hepatocelIular disease.

	Intravascular	Extravascular
Peripheral smear	schistocytes	spherocytes
Haptoglobin	decrease/absent	mild decrease
Urine hemosiderin	++	negative
Urine hemoglobin	++	negative
Direct DAT	usually negative	++++
LDH	increase	increase

Bite cells are present in G6PD deficiency



blister cells in G6PD deficiency