PROF.DR.H.GUSBAKTI,MSc,PKK,AIFM

PEMENUHAN DIRIFULFILLMENT

PELAKSANAAN YANGPENUH SEMANGAT

PASSIONATE EXECUTION

SUMBANGAN YANG BERMAKNASIGNIFICANT CONTRIBUTION 8TH HABITS

STEVEN R COVEY

MEDS

MOTIVATIONEDUCATIONDEDICATIONSKILL

KENAPA MEMILIH MENJADI DOKTER

TIPS

TRUST INTEGRITY PROACTIVE SOLUTION

TAHU , MAMPU DAN MAU

TEKNIK-TEKNIK UMUM BELAJAR1. PERENCANAAN2. MENERIMA PELAJARAN DI KELAS/

format catatan tehnik 5R ,RECORD,REDUCE,RECITE,REFLECT AND REVIEW/TEMUKAN SENDIRI CARA

3. MEMBACA BUKU4. MENGERTI BUKAN MENGHAFAL5. MEMBUAT RINGKASAN6. MEMBUAT KATA KUNCI7. BELAJAR BERSAMA

1. PERENCANAAN

BELAJAR

Fungsi Perencanan Belajar : Membimbing diri kita belajar secara terarah dan produktif

PERENCANAAN BELAJAR

PERLUKAH?

Teknik PerencanaanMenyusun Jadwal :-Menetapkan tujuan-Waktu produktif-Kapan kita belajar-Membuat jadwal-Rekreasi & kegiatan di luar belajar

PEMBUATAN JADWALFUNGSI Membantu

penggunaan waktu seefektif dan seefisien mungkin

Melatih untuk selalu siap dg pekerjaan berikutnya

PERHATIKAN Setiap mata kuliah

harus tercantum dlm jadwal

Alokasi waktu bukan berdasarkan mata kuliah favorit

Waktu antara

PEMBUATAN JADWALLangkah-langkah penyusunan jadwal Hitung jumlah jam belajar dan waktu

yang tersedia Isilah waktu-waktu rutin yg diperlukan Isi waktu-waktu janji (dengan

pembimbing,dll) Tentukan waktu belajar

(sebelum/setelah kelas?) Sediakan waktu cadangan/waktu bebas

MEMBACA BUKU

Teknik Membaca Bukua.Tetapkan tujuan

Apa yang hendak dibaca Untuk apa kita membaca

b.Skimming/ SEPINTAS LALUc.Dapatkan Ide Pokok dan Rincian Pentingd.Menggunakan mata fiksasi mata

MENINGKATKAN KEMAMPUAN MEMBACA

a. Jangan bicara

b. Membaca satu unit pikir

c. Latihan membaca cepat/200 kata-menit – Lewis 1986 – dapat ditingkatkan sampai 500kata/menit

d. Teknik SQ3R,SQ4R,OK4R, dan PQRST

e. Menggaris bawahi

f. Menghindari lelah dan bosan

Membaca sesingkat mungkindaya serap tinggiSQ4R/MILLERSURVEYQUESTIONREADRECITEREVIEWREPEAT

OK4R/WALTER PAUKOVERVIEWKEY IDEASREADRECALL/RECITEREFLECTREVIEW

LANJUTAN………..

THOMAS F STATON

PQRSTPREVIEWQUESTIONREADSTATETEST

OHIO UNIVERSITY

SQ3RSURVEYQUESTIONREADRECITEREVIEW

BUKU 100 HALAMAN

Hari pertama 1 jam hal 1-50Hari ke dua halaman 1 – 75 = 1jamHari ke tiga 1-100 1,5 jamDiperlukan strategi untuk

meningkatkan kemampuan membaca dengan tehnik tertentu sehingga komponen yang dingat semakin banyak.

MENGERTI BUKAN MENGHAFAL

MENGHAFALSALAH?

Menghafal Tanpa

MengertiSering

Menghafal dengan

Mengerti

Lebih sulitBuang waktu banyakPelajaran tetap tidak dikuasai

Exercise –

Other Mechanisms of Drug Antagonism

Not all of the mechanisms of antagonism involve interactions of drugs or endogenous ligands at

single type of receptor. Indeed, chemical antagonists need not involve a receptor at all. Thus, one drug may antagonize the actions of a second drug by binding to and inactivating the second drug.

For example, protamine, a protein that is positively charged at physiologic pH, can be used

clinically to counteract the effects of heparin, an anticoagulant that is negatively charged; in this

case, one drug antagonizes the other simply by binding it and making it unavailable for interactions with proteins involved in formation of a blood clot.

The clinician often uses drugs that take advantage of physiologic antagonism between endogenous regulatory pathways. For example, several catabolic actions of the glucocorticoid hormones lead to increased blood sugar, an effect that is physiologically opposed by insulin. Although glucocorticoids and insulin act on quite distinct receptor-effector systems, the clinician must sometimes administer insulin to oppose the hyperglycemic effects of glucocorticoid hormone,whether the latter is elevated by endogenous synthesis (eg, a tumor of the adrenal cortex) or as aresult of glucocorticoid therapy.

Con’t

In general, use of a drug as a physiologic antagonist produces effects that are less specific and less easy to control than are the effects of a receptor-specific antagonist. Thus, for example, to treat bradycardia caused by increased release of acetylcholine from vagus nerve endings, the physician could use isoproterenol, a -adrenoceptor agonist that increases heart rate by mimicking sympathetic stimulation of the heart. However, use of this physiologic antagonist would be less rational—and potentially more dangerous—than would use of a receptor-specific antagonist such as atropine (a competitive antagonist at the receptors at which acetylcholine slows heart rate).

Con’t

Signaling Mechanisms & Drug Action

Until now we have considered receptor interactions and drug effects in terms of equations and

concentration-effect curves. We must also understand the molecular mechanisms by which a drugacts. Such understanding allows us to ask basic questions with important clinical implications:

• Why do some drugs produce effects that persist for minutes, hours, or even days after the

drug is no longer present?

• Why do responses to other drugs diminish rapidly with prolonged or repeated

administration?

• How do cellular mechanisms for amplifying external chemical signals explain the

phenomenon of spare receptors?

• Why do chemically similar drugs often exhibit extraordinary selectivity in their actions?

• Do these mechanisms provide targets for developing new drugs?

Most transmembrane signaling is accomplished by a small number of different molecular

mechanisms. Each type of mechanism has been adapted, through the evolution of distinctive proteinfamilies, to transduce many different signals. These protein families include receptors on the cellsurface and within the cell, as well as enzymes and other components that generate, amplify,coordinate, and terminate postreceptor signaling by chemical second messengers in the cytoplasm.

This section first discusses the mechanisms for carrying chemical information across the plasma

membrane and then outlines key features of cytoplasmic second messengers.