100% satisfaction guarantee Immediately available after payment Both online and in PDF No strings attached
logo-home
Summary Pathophysiology Rapid Revision Krok 1 $3.21   Add to cart

Summary

Summary Pathophysiology Rapid Revision Krok 1

 28 views  0 purchase
  • Course
  • Institution

In this file you will find a Rapid Revision Summary by Medic Mukul, for the Pathophysiology part of Krok 1. A part of the summary is based on most frequent asked questions as well as ministery questions.

Preview 3 out of 7  pages

  • May 2, 2023
  • 7
  • 2022/2023
  • Summary
avatar-seller
Dathophysiology

Rapid Revision KROKI




Minna Mamik
@ Medic Mukul

,Minna Mamik
Anemia
colour Index
>Hereditary hemolytic Anemia (mutation present
=
0.9-1.0

Hypockcomic Anemia Membrane
defects Ameditary Spherocytosis Minkonsky
2
1. -> c


shaffered Syndr
Normocytic Anemia Based on MCV N 00-100f1
=


2.
Enzyme Deficiency ->
G-G-PD
deficiency
Hyperchromic Anemia ~ Mean Capusatan Volume
Hexokinase deficiency
>Hypochromic Anemia -
CI o.q or less than do MCV 3.
Hemoglobinonopathics-> Sickle all Anemiaz
Glutamate repla
Oh

Thalassemia
MiocoCytic Anemia
-> peripheral
newio-
by Valine
pathy
I
S-Sideroblastic Anemia -t Bs (Basophilic
Stippling Seen)
Extravascular Micovas
-- Icon
deficiency Anemia (Nail brittleness & Hainloss)
hemolysis -


spleen hemolysi
stick to b
CoutRBC)
-




T- Thalassemia (blood doesn't
make Hb) vessels
autosomal
enoughinherited
zeccesive
A -
Anemia of Chronic Disease (such as Kidney Diseasel Hereditary Sphereocytosis -
Autosomal
(membranopadty)
Dominant

L- Lead
H ↳due do membrane protein defect
poisining
GSphere talenen ↳ Spectzin, Anchyzin, Band cell

(SAB)
& ↳Extravascular
>Namocydic Anemia MCV 80-100 cl 0.9-1.0 hemolysis
=
-




GGPD deficiency Anemia x-linked Recessive ⑭P
Aplastic Anemia
(bylomyledenBoneMaaree
·
-




G-6 -

P
chronic Renal Failure ↳Accumulation of H202 (fee Radical)
exhe-sp
·




in Risc x

-

·
Anemia of Chronic Disease
Hemolysis oxidative stress 6-phosphog
·


Hemoytic Anemia

during ↓
conate


RBC Destruction Ab Denaturation
↓ ↓
Anemia
>Macrocytic -
MCV> 100 & CI> 1.0 intzavascular
Deoxygenated pencipatation
hemolysis of Hb
L- Liver Dysfunction (Heinz bodies)
Neural ↓
A -




Hypothyzoidism Tube
↑ Defect pass through spleen &
(Dueto VitBiz/Badef) Destroyed by splenic Macoph
M
-Megaloblastic Anemia >Factas
causing hemoysis ↓
↳ Howel Bodies in
GGPD
Jolly seen
Cell formed
c -




Cytotoxic drug - chronic infections
Anti malarial
Bite

-


Drugs like
Extravascular hemolysis
-Fava beans


poikilocydosis -


change in shape of RBC (pp) Note;GGPD, Sickle cellAnemia & Thalassemia

(pizal
Anisocytosis -




Change in Size of RBC (2a) protective against plasmodium
Cresistand to malaria)
Pecusa of RBC ->
Rediculocytes (NON -
Nucleated)

>Autoimmune
Hemoydic Anemia


type
Periphera) finding
Smean
hypersensitivity
It reaction

nemia Microse Andibodies proteins
Due do
against RBC membrane
- ->




>Macrocytic Anemia -
Macco cells

Spherocytes - in
Hereditarysphereocytosis, Microangiopathic hemolytic Anemia

(NO Centralpallor)
Syndrome (Hus)

autoimmune
hemoydic An. Hemoyhic Uzemic
↳ Thrombodic
>Polychromasia ->
Hemoydic Anemia
Thompocytopenia purpura
↳ Disseminated Intravascular
> Bite cell ->
Glucose -


6.phosphate Deh.
Coagulation
Heinz Bodies. Deficiency Anemia

↳ composed of
We See
Schistocyte/helmet/Fragmental RBC

denaturated Hb
percipated >paraoxymal Noctural
Hemoglobinuria
>Schistocyte/ helmet I Microangiopathic Hemolytic ↳
Only Amhemolytic Anemia
Anemia
Fragmented RBC ↳ More
hemoglobin (Abrucial
Cell & inThalassemia ↳ (HRBC)
>Target Pancytopenia
↳ Microcytic
Basophillic Stripping hypochromic ↳
erythroctes
t &↑ Ab
Red Cells
↳ MCC Fe
of death=
overload due to repeated Transfusion

, Minna Mamik

Leukemia - Cancer of blood-faring dissue Acute
Myeloid Leukemia
(including bone Marrow &
lymphatic System)
<15-45
yes

Hemadopoiesis -> Formation of Blood Cells . Gum
hyperplasia/Bleeding
↳ liver BR & Liver, Bone Marow)
Coagulation (DIC)
(yolk sac -Disseminated Inteavascular
ardweek 3rdmoth 4th month just before
Birth


Hemapoltic Stem Cell >Chronic Leukemia -

Neoplastic peration of Mature
Common Myeloid Common' lymphoid Circulating lymphocytes, characterised
Drogenita peogenita. by high WBC Count
I
I T -
&
B-lymphocytes
>Erythoblast-> RBC & Chronic Myeloid leukemia

>Megakaryoblast platelets ->
NK cells

Eldery people
*ByodMaromslauk
>Myeloblast >Massive
hepatosphenomegaly Seen

↳ of
Neutrophils Babeseen
.


cytoplasm -



>changed chromosome -
22 (philadelphia chromosome

·

Eosinophils -


Binudeate/spectac shaped Nuclei >↑ No. of all
mydoid linege cell (Madue Myeloid)
granules in Cytoplasm
Brick Red
·
Basophils
-4
Basophils 1 Both are absent in Reactive
z
large Bluish geanues in
cytoplasm
which obscure the nucleus -
tcanslocation Neutrophilic Leukocytosis (*nautzophil
9 h&22nd CLeukemoid Reaction)
t




>Monoblast ->
Monocytes-largestcell, kidney shaped nucleus,
Agranulates (donthave granules)
Chronic
lymphoid leukemia Goyrs)
↳ Neoplasticproliferation of mature
monocytes
B-cell
I Agranulogy en

↳ Blood Smear -> 4
lymphocytus
Normal level CD34 -
MackerfaMSC) Smudge & Botkin
Cells
WBC -> 3 9x109/L hematopoletic stem cell
↳ of lymph
-




6x10/ Involvement node leads togeneralised
RBC
-


=
4 -




lymphadenopathy (Small lymphocytic leukemia)
(cancuous/abnormall cells)
Neoplastic lessions of WBCs
can become
leukemia L
can become
>
Lymphoma Acte Chronic

Involvement of Bone Mariow/ More Systemic/c
Blast > 30% >pediferation of
mature cell
Smeal Tissue Involvement
Periphezal >WBC <50x10"/ >WBC<50x109/

of
like lymphnode/spediferation
Lympho-&Ryeloblast
>promyelocytes
Spleen
Leukemia
>Acute

Mariow/Peripheral
Lymphoma
↳ 30% blasts in Bone Blood

lymphogranulo-
Lymphoblasts Mycoblasts Hodgkin's lymphoma metosis
Non-Hodgkin's lymphoma
-Smallen in Size
-Langen in Size 1) Bimodal age distribution 1) Can Occur at
any age
-Geanules present
(15-20 yes, elders)
>No Granules 2) Generalised lymphadeno-
Guical,
padhy
Ave Mods abscent & Auns mods present 2) lymphadenopathy
(Hall mark of Ryeloblasts)
>Coarse/dumped Chromatin Contagious Spread
3) 3)
Non-Contagions spread
>Open up/Homogenous
Chromatin 4) Reed-Sterberg
aka
alls pt.
Acute
lymphoid leukemia -
ALL owl's
eyes cells

>MC Cancer in Children (2-9yrs)
>t Number of NBC - ↑ infections Lymphogzanulomadosis one of lymphadenopathy disease


st
platelets 2 Reed -



Steenberg cells


Idepatosplenomegaly 3 Necrosis in Immune
Ozgans
· TdttVe (RackenfaAll) 4
parphyzidic Spleen

The benefits of buying summaries with Stuvia:

Guaranteed quality through customer reviews

Guaranteed quality through customer reviews

Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.

Quick and easy check-out

Quick and easy check-out

You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.

Focus on what matters

Focus on what matters

Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!

Frequently asked questions

What do I get when I buy this document?

You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.

Satisfaction guarantee: how does it work?

Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.

Who am I buying these notes from?

Stuvia is a marketplace, so you are not buying this document from us, but from seller minoo. Stuvia facilitates payment to the seller.

Will I be stuck with a subscription?

No, you only buy these notes for $3.21. You're not tied to anything after your purchase.

Can Stuvia be trusted?

4.6 stars on Google & Trustpilot (+1000 reviews)

67474 documents were sold in the last 30 days

Founded in 2010, the go-to place to buy study notes for 14 years now

Start selling
$3.21
  • (0)
  Add to cart