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Summary Biochemistry Rapid Revision Krok 1 €0,00

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Summary Biochemistry Rapid Revision Krok 1

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

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  • 2 mei 2023
  • 7
  • 2022/2023
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Door: harmdhal • 1 maand geleden

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minoo
Biochemistry
Rapid Revision KROK I




Minna Mamik
@ Medic Mukul

, Minna Mamik Monohydrofoic ->
Tetzahydrof. -DNA

Steatorchea
1) -
Fat instoo (Fat Bile] =




Dihydrofolate
7) Reductase =) helps in DNA Synthesis c Mononudeoti
Synthes
Biliary Tre Requires Bar Follic Acid
->



as cofacto


inhibited Methotrexate
->
by Dag
Bite is secreted ↳inhibits DNASyn. &Bg
liver
by Inhibits
Anti-Cancer
MAF- THE
drug
=>




Bile is stad & 0) Amatidine present =
in Mushroom, Causes
Mushroompoisining

i n Gall
concentzate
(Death (up) Inhibits RNA
polymerase II (inhibits transcription)
->

Bladder


9)Porphyria/Vampire
disease HEME
-



Synthesis
concentzate

stage of De maisicatesphinter te
-
open dag
->
takes place in Mitochondria &
Cytoplasm of liver
Bile ing of oddi
Duodenum URopophyzinogen co-II
Synthase enzyme deficien
->


on
A Maja papillae 4 U-p-co-
->
Pink wine
<opening)
Longitudinal
Folds present 10) Duchenne Muscular Dystrophy - Wheel chair
disease

Bile ductobstruction -
Bile problem =

NO FAT ↳ Absence of Dysteophin & Creatine Kinase 4tmm

Beckers Muscular
O FAT ABSORPTION
N

11) Dystrophy -
Bad
Dystrophin
Becomes 1 Fat Soluble Vitamin Messengel
10 hormones =




Essential (cannot absorb) ba that dus wat Pa
(musttake i it
A, D, E, K 12) Secondary Messengen [Amp] (transpat harmones from
(watchmen) 1-CAMP-Lipase,
-
etc. membrane to nucleur m
2) Galactosemia individual not able to metabolize Galactose 2 cGMD-NitricOxide & Azterial Natudic Fadez
-
-




(AN
A
Genetic Disorder-Galactose I phosphate Uridy Transferase 3-1P3 -
Iositol Tiphosphok (uses Cat
↳ (deficiency) ↳
Typical Galactosemia ee
Angioten Is
cause used
by e.g. Epinehren
O

Classical Galactosemia 7 -
Di
acys glycand in vasoconstride
ves




-> Oil Drop Catart is seen

3) Eructosemia Aldolase
Benzyme deficiency [FAB] B3) DNA Enzymes
=




n




mainly liven, kidney & intestine 1 Helicase
unwinding the 2 strands
->
in -
->




4)
Glycogenesis ->
Synthesis of Glycogen (Branched 2-Topoisomerase -
Super Colling
Basal alle
polysacharide a
storage form in animals)
3-ligase -
Helps in
joining Con dissue

genesis -




farming ↓ ↓

lysis-breakdown
->
Enzyme;Glysogen Synthese 4 - Endonuclease - DNA Repair
Regeneration
Insulin stimulates ↳ Endonuclease
->
glycogenesis, activates deficiency cause Xenoderma
pigmentosa
↳ Glucose
↓ By UV-midiation.



5) Glycogenolysis Breakdown of Glycogen (4) Phospholipase A2-> helps in Azachinoidic Acid
Synthesis
-




From phospholipids through Cox &
goes
->
Enzyme; Glycogen phosphaylase [Gp] 15) Antioxidants Lox
pathway
->
Glucagon stimulates Glycogendysis Vitamins - VitA
AsCE

MC ARDLES Disease
Deficiency
=



of GP in Muscles vit C

types glucogen stage
disease vitE (mostpotent antioxidant)

HER'S Disease
Deficiency
=


of Gp in liver (type 6)

Proteins -
1 Transferrin (transport
iron fel
C42+
6) Gluconeogenesis -

Formation of Glucose from other than Carbo- 2 Guloplasmin staes & transpats
copper from li
hydrate of body
into bloodstream to part
->

enzyme;
Glucose 6 phosphatase (mainly present ↳ deficiency-> Wilson Disease
in liver go-g5y)
VON GIRKE
Disease 3 Albumin-> most Abudant protein Blood
Type Iglucogen stage disease sy.
kidney in
-




->
Absence of Glucose 6 phosphatase ↳ fluid from leaking out of bloodves
prevent
&transpats, hamones, vit & enzymes
4 Glutathione detoxification->

, Enzymes 1
Super Oxide Dismudase Q incase of Wound, Oxidative
Recaboxylation -




Scoenzymes used
we will use H202 ↓
Liberate CO2
2
Hydrogen penoxidase <
(Thiamine
Tpp pyrophosphate) B,
Catalase
Hase, H20+02 >COA
(in skin)

3 active fam of Bs
↓ 00
fams bubbles
4 Glutadhione Denoxidase =
>lipoamide (lipoic Acid) -
inhibited
by
of bact.
anemy Sodium Azsenat
3 Glutathione Reductase >NAD Be
+




an >FAD
septic
B2

↳ Examples; alls-I
↓use
16) Blocked
ATP
=>Resting Membrane Potential will disappear Pyzuvate
Dehydrogenese complex (PDC)

Branched chain Kedo
17)
Jaundice Dehydrogenase(BckD
of Alpha keto Glutamate
Hemolytic jaundice -
Breakdown RBC
Dehydrogenase (A-kGDH
Aka prchepadic jaundice
I ·Unconjugated/indirect / Non soluble
Bildwin Enzymes &
Prosthetic Go
t

- Dack stod/Feces & Uzine Mostcommon -> Metals
(morganic ions)

Hepatic jaundice -


UDP Glucozyne Transferase enzyme e.g Tyzosinase
-
Cult
conjugation ↓
in liver
Cunconjugated J.) deficiency convents indirectbillizbin Carbonic anhydrase - Int
into direct bilizubin
Int
Carboxypeptidase -





e.g. Crigle Najlar Lyndrome Tratment Metalloenzymes CAg
phenobabitol
Carbonic
anhydrase
Obstructive
a Mechanical
Jaundice -
AKA


↳ ediology:Cholelidhiasis (FAT in stock) gallbladen
Posthepatic].

stone
Carboxy peptidase
Alcholo
Dehydrogenese
I all
enzymes



/
need en2t
Alkaline
-> Ma
Conjugated/soluble/Direct Billizubin phosphatase
. Ala Dehydrogenase
10) Methylation -
Done
by Methionine (Amino Acid) >Lactate
Dehydeogenase

(Methylatingagentasphetic
and Choline.
( Absence heads liven. >Kinases
I
to
->
Fatty Choline(
>Mutases need

Mgation
19) Carbon Labelled Glucose -


Palmitic Acid CIS
aids
Fabdy
Carbon
compounds
S Enolases

Glucose 6-phosphate
-
~
20) Enzymes -



Allenzymes are
proteins except Ribozymes



2
Apoenzyme -
of enzymes
proteinous part ~Tyzosinase
Cofacta, Coenzymes, prosthetic group Non
-

proteinous <Cytochrome Coxidase (complex(v)
part

Holoenzyme ->
protein Non
+


protein
part Lysyl oxidase all need




~
cuztion
Superoxide dismutase cooper




D
Enzymes &
Coenzymes By By
vitB, -Tpp >L- amino oxidase


D Dehydrogenase -
NAD+, FAD B -


FDP
By NAD
2) Kinases anthine
-




ATP X Oxidase
2
-




toofan
Transketolase (B,) sulfide
~allnedee
3) - Thiamine , Oxidase
BI
Carboxylase Biotin, VitH, ATP
4) -




>Dinitzogenase
5) Decarboxylase
↳ Simple Decarboxylation -




PLP (vitBs)
Histamine & GABA Synthesis
e.g
->



Histadine Histamine
Minna Mamik ,

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