Hemohrrage Flashcards
نمت وأدلج الناس؟
Goldblatt hypertenion is ?
Renovascular hypertension due to occlusion of renal arterires and releasing renin >ANg2
ادع العزيز الحكيم المجيب الرحيم
Monogenic hypertension ?
hyper tension due to one gene mutation casuing na water reabsorption
Serious adverse effects of ACEI MENTION
• Reversable renal impairment if taken in renal hypoperfusion (High renin states)
- Bilateral renal artery stenosis # (use in unilateral)
- Extensive doses of loop diuretics (stop 24 hours before ACEIs)
• Bone marrow depression
• Fetotoxic (in 2nd & 3rd trimester) and teratogenic (1st ) # Pregnancy
Most Serious:Most common: ADVERSE EFFECTS OF ACEI ? MENTION
Most Serious: Angioedema (Rare but fatal) Most common: Dry cough (due to ↑BK)
④ Less common adverse effects of ACEI Mention ? !
• 1st dose hypotension : start with low dose at evening • Hyperkalemia مين مع) β Bs or K+ sparing) • Hypersensitivity reactions: rash,… • GIT upset: ANVD & taste disturbances
ARBS classify .
Block AT1 receptors which mediate most of
pathological CVS effects of Ang II
2. Spare AT2 receptors → VD & antiproliferative effect
Define hemorrhage.
It is loss of blood classified into
acute hge sudden loss of great amount of blood at one time by trauama or surgery
casuing hypotension and syncope
chronic hypotension ?
repeated loss of small amounts of blood for along period of time this leads to hypotesnsion and anemia and may refer to dangerous diease
tips of the amount of hge is less than 10% no change in COP OR ABP
LIKE BLOOD DONATION
If the amount of blood lost 10-20% this leads to dec cop and compensatory mechanisms
the amoun t>20% this leads to uncompenatsion nedd treatment hemohragic shock nedd treat
>30% uncompenastaed cannot be treated
ولقد كنت في حلاوة طلبي للعلم ألقى من الشدائد ما هو عندي أحلى من العسل ؛ابن الجوزي !
What is the aim of compensatory mecanisms and its types ?
Treatment of drop in ABP
Treatment of drop in Blood volume
long and short term mechanisms
Compensation mechanuisms vary from one to another even in the same blood loss
ARBS FAMILY MENTION
Members Sartan family
Old: Valsartan -Losartan
New: Candesartan - Eprosartan - Telmisartan
The degree of shock depedns on ?
1- rate of bleeding
2- the adequacy of compensatory mechanisms
3- course and mangement of case
Short term mechanisms in restoring ABP in Hge?
Inhiniton of Baroreceptors impulses due to hypotension sensation !
Stimulation of chemoreceptors
stimulatrion of CNS ischemic respone
all cause stimulaiton
of VMC casuing increasr VC of peripheral
and increasing cardiac propertirs
-angionteni2 and Vasopressin due to renal hypoperfusion renin !
Short term compensatory mechanisms in restoring blood volume ?.
Capillary fluid shift and Labile tissue and liver proteins to plasma increasing osmolarity and absorption from ISF AND Contraction of splenic capsule
Long term compensatory mechanisms in ABP Restoration ?
Renal and hormonal Renal لما يقل ضغط الدم يقل الفلترة في الكلية فيحافظ علي حجم بلازما الدم hormones Reinin angiotensin ADH Aldosterone Cortisol VC vasular reactivity to sympatho and na water retention
Long term compensatory mechanisms in Restoration of Blood volume?
1- thrist ang2 and hormonal water conservation
2- plasma proteins replaced by liver
3-RBCS replaced by Bone marrow
Barorecptors in response to the Acute Hge?
it decrases it discharges to the VMC casuing its stimlation and increasing sympathtaic effect on
1- perepherial areterioles casuing vc and increase tpr and abp
with exception brain and heart !! the skin become cold and pale
this leads to vc of renal arterirs and decrasing urine formation
2-venoconstrivtion increasing vr and cop despite blood loss
3- increasing cardiac properities incresing cop and abp
lead to rapid weak pulse rapid due to HR increased and weak due to increased DP due to increas TPR
4- increasing Adrenal medulla release of catecholamine support all the functions mentioned above
and helps in the reticular formation casuing increased musle tone and VR and cop AND ABP so the patient is restless
The importance of decreased pulse pressure by the baroreceptor reflex?
the depressor are will remain depressed as well as pulse pressure is waekened
chemorecceptors in acute Hge show relation ?
Chemoreceptors stimulated in case ol apb < 80 mm Hg by hypxoia hypercapnia and acidosis lactic acid
and by po2<60 mm Hg and this leads to stimulation of VMC
INCREASING VC AND C PROPRETIES AND ABP
decreasign Vagal tone
Stimulation of respiratory center casung tachypnea rapid shwalloing breathing increasing VR by thoracic pump
CNS ischemic reflex and acute Hge ?
It depednds on decrasign BP< 60 mmHG
AND This leads to ischemia of Brain and VMC
casuing Stimulation of VMC to survive
and his VC and cardiacproperties to increase bp 5-7 minutes to increase bp and cereberal perfusion
Short term horomnes in acute Hge ?
In case of Hge there is Renal hypoperfusion casuing more reinin to release from juxta glomerular appartus and this form in the end Angiotenisn 2 which is ?
Vasoconstrictor Arteriolo and Venulo increasing TPR AND VR
Aldosterone salt and water retention
AHD vasopressin from pp leading to retenriton of water from DCT and collectiong duct and may casue VC IN V1 IN HIGH DOSE !
Thrist sensation
Short term mechanisms correcting bv in acute Hge ?
the capillary shift
لما يحصل ضيق في الشرايين فده بيؤدي الي نقص ضغط الشعيرات فتسحب الماء من النسيج البيني لزيادة الضعط جواها
proteins from liver and labile tissue
RBCS from splenic capsuel contraction leading to increae blood volume
Long term mechanisms in correction of ABP ? \
Renal and hormonal
Renal
نقص الضغط يقلل الفلترة يقلل تكوين البول يحافظ علي الصوديوم والماء ويزود الحجم الدموي والرجوع الوريدي والمخرج القلبي و الضغط الدموي
والعكس !
Hormonal Renin angiotensin system ?
Renal hypoperfusion leads to more reinin increasse from JGA and this will lead to ?
ANG2 MOST POTENT VC
Artreiolo and venulo constriction
Thris senstation incr bv
Aldosterons salt water retension
corisol from adrenal cortex same mechanism
ADH vasopressin DCT AND CT prevent water excretiion
vc in high dose ?! yes
Long term regulatin of BV IN HGE?
the plasma volume is restored 12-72 hours by thrist by ang2 and Alodsterone and ADH AND CORTISOL
The plasma proteins come from liver and labile tissue
the plasma RBCS repleaced by bone marrow !
INDICATIONS OF ARBS MENTION
AS ACEI. Used alternative if the patient can’t tolerate ACEI (e.g. dry cough)
1. Hypertension
2. Heart failure: all cases & all stages decrasing preload and afterolad
3. Acute MI: (in first 24 hours with β-blockers, aspirin and fibrinolytics) →
• ↓ Sudden death (prevent arrhythmia 2
ry to hypokalemia and ↑ sympathetic activity).
• Post MI: ↓ aldosterone induced remodeling & prevent Heart failure
4. Nephropathy: diabetic or non-diabetic
